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ME/CFS is a chronic illness that profoundly affects people’s quality of life. Its hallmark symptoms include debilitating fatigue that is not relieved by rest, cognitive impairment often referred to as “brain fog,” sleep disturbance, and post-exertional malaise. Post-exertional malaise is a phenomenon where even minimal physical, mental, or emotional exertion can trigger a significant worsening of symptoms. This can occur hours or even days after the activity and may last for days, weeks, or longer.

Kingdon and colleagues note that the condition is complex, with no definitive diagnostic test and no effective treatments to date; the disease just has to be managed. Causes of ME/CFS remain unclear. Some evidence points to a genetic predisposition. For many people, ME/CFS is precipitated by an infection (including COVID-19 infections), vaccination, or physical trauma. And a number of abnormalities involving the brain, immune system and muscle energy production appear to be involved in perpetuating ME/CFS.

Historically, ME/CFS has been diagnosed only after four to six months of persistent symptoms. The new NICE guideline recommends a diagnosis within three months, provided symptoms such as post-exertional malaise are present and other conditions have been ruled out. Early diagnosis is critical, as it allows healthcare providers to offer timely advice on managing symptoms and avoiding activities that might exacerbate the condition. For instance, patients are encouraged to pace themselves, a strategy known as energy management, which involves balancing activity with adequate rest to prevent overexertion.

A major change in the new guideline is the rejection of graded exercise therapy. For decades, graded exercise therapy was widely prescribed based on the idea that patients needed to incrementally increase their physical activity to regain strength. However, for many with ME/CFS, this approach has proven to be harmful. Surveys involving over 15,000 patients reveal that more individuals report harm than benefit from graded exercise therapy. Patients often experience severe relapses after following these programs, as their energy limitations are ignored.

Similarly, the use of cognitive behavioural therapy (or CBT) as a “cure” for ME/CFS has been reevaluated. While CBT can help patients cope with the emotional and psychological challenges of living with a chronic illness, it should not be offered as a treatment to address the underlying condition. The guideline now emphasises that care must focus on symptom management rather than attempting to “fix” the illness through inappropriate methods.

Kingdon and her colleagues emphasise the need for a personalised approach to managing ME/CFS. The new guideline calls for a multidisciplinary team of healthcare professionals to collaborate on individualised care plans. These teams should include physicians, physiotherapists, dietitians, occupational therapists (and psychological support where required) – each contributing their expertise to address the diverse symptoms of ME/CFS.

For example, patients with severe fatigue may benefit from occupational therapy to find ways to conserve energy while performing daily tasks. Those with chronic pain might need tailored interventions such as pharmacological treatments or strategies to manage discomfort without overexertion. Patients with dietary challenges, such as difficulty swallowing or maintaining proper nutrition, may require input from a dietitian to prevent malnutrition.

Importantly, the guideline also recognises the fluctuating nature of ME/CFS. A patient’s symptoms may vary from day to day or even hour to hour. This means care must be flexible and adaptable, allowing for adjustments as needed. One of the most striking aspects of the new guideline is the emphasis on addressing the prejudice and disbelief many patients face. People with ME/CFS often encounter scepticism from healthcare providers, employers, and even friends and family. This can compound their suffering, leading to feelings of isolation and a loss of trust in medical systems.

The NICE guideline acknowledges this history of stigma and encourages healthcare providers to approach patients with empathy, validating their experiences. It highlights the need for supportive, trusting relationships between patients and their care teams. The impact of ME/CFS extends far beyond physical symptoms. Many patients are unable to work, attend school, or participate in social activities. The new guideline stresses the importance of providing support for education and employment, including reasonable accommodations such as flexible hours or remote work options. For those who are severely affected, home visits and disability aids such as wheelchairs may be necessary.

Patients are also advised to prioritise rest and recovery during relapses, which are periods of worsened symptoms triggered by overexertion or illness. Clear guidance on how to manage these flare-ups can empower patients to stabilise their symptoms and gradually resume daily activities.

While the NICE guideline applies to ME/CFS patients in the UK, its influence is being felt internationally. By rejecting outdated and harmful treatments such as graded exercise therapy and recognising post-exertional malaise as a cardinal symptom, they align with recommendations from global organisations such as the U.S. Centers for Disease Control and Prevention. This marks a growing consensus in the medical community to prioritise evidence-based, patient-centred care for ME/CFS.

The NICE guideline represents a turning point in the care and understanding of ME/CFS. By championing early diagnosis, rejecting harmful practices, and promoting individualised, compassionate care, they have given new hope to the millions affected by this debilitating condition.

For patients and their families, this guideline provides a blueprint for better care, one that acknowledges the reality of their illness and offers practical, evidence-based solutions. While there is still much to learn about ME/CFS, this progress is a significant step toward improving the lives of those who endure its challenges every day.

Cholangiocarcinoma arises from cells in the bile ducts, which are small tubes that transport bile, a digestive fluid that breaks down fats, from the liver and gallbladder to the intestines. These bile ducts can be affected by cancerous changes in two main regions: the intrahepatic area (which is inside the liver) and the extrahepatic area (which is outside the liver and closer to the intestines). Although this cancer is rare, making up only 3% of gastrointestinal cancers diagnosed in the US, it is among the most aggressive cancers found in the gastrointestinal tract, and underlies approximately 20% of the deaths caused by gastrointestinal cancer. Its late diagnosis is a key reason why effective treatments are urgently needed. As a targeted therapy, pemigatinib focuses on a genetic characteristic of some cholangiocarcinoma cells. This involves mutations or rearrangements in the FGFR2 gene, which are found in around 10-15% of patients with intrahepatic cholangiocarcinoma. This gene typically helps to control cell growth, but in these patients, it malfunctions, allowing cancerous cells to grow uncontrollably.

Pemigatinib works by blocking this dysfunctional FGFR2 pathway. This “targeted” approach represents a shift away from traditional chemotherapy, which generally affects both cancerous and healthy cells, leading to a wide range of side effects. Targeted therapies such as pemigatinib, on the other hand, are aimed specifically at molecular abnormalities in cancer cells, reducing the overall damage to healthy cells and often resulting in fewer side effects for the patient.

Pemigatinib has shown promise in cholangiocarcinoma patients with FGFR2 abnormalities in previous clinical trials. However, Dr. Saverno and colleagues assessed how effective pemigatinib is in real-world medical practice, examining data from 120 patients treated with pemigatinib by oncologists across the United States. This “real-world evidence” is crucial because while clinical trials are conducted in highly controlled environments, real-world settings provide a broader perspective. Patients in everyday practice may differ from those in clinical trials; they may have additional health conditions, belong to various demographic groups, or face challenges in following strict treatment regimens. This diversity can affect how well a drug works and what side effects it might cause.

The findings are promising. Dr. Saverno and colleagues found that among the patients treated with pemigatinib, approximately 59% responded positively, meaning that their cancer showed either a partial or complete reduction. The median progression-free survival, which indicates how long patients lived without their cancer worsening, was 7.4 months. These findings support the clinical trial results demonstrating the clinical benefit of pemigatinib among patients with cholangiocarcinoma.

Many cancer treatments are discontinued by patients as the side-effects become intolerable. However, this study found half of the patients were still taking pemigatinib by the end of the 6.5-month median follow-up period, highlighting its potential for sustained use.

For patients to benefit from pemigatinib, they first need to undergo genetic testing to identify FGFR2 mutations. Among the population of patients who had received pemigatinib for the treatment of cholangiocarcinoma in Dr. Saverno’s study, over 90% of patients who were tested showed FGFR2 mutations, and this testing played a crucial role in determining eligibility for pemigatinib. Typically, next-generation sequencing was used, a powerful technique that analyzes DNA to identify genetic mutations and helps doctors match patients with targeted therapies. The study highlighted that most patients with FGFR2 mutations were prescribed pemigatinib as a second-line therapy, meaning they received it, according to the FDA approved indication, after initial treatments such as chemotherapy proved insufficient.

One important aspect of this study is that it included a racially diverse patient group, with participants from different ethnic backgrounds and regions. This diversity matters because responses to cancer treatments can vary across populations, and the inclusion of varied demographics makes the study findings more widely applicable. More than half of the study participants were White, while 20.8% were Black or African American, and 19.2% were Hispanic. These latter two groups are often underrepresented in clinical trials. This diversity is particularly valuable for assessing how different populations respond to pemigatinib and offers insights into its effectiveness across a broad range of patients.

This research highlights the growing importance of precision medicine, an approach that tailors treatment to a patient’s specific genetic profile rather than relying on one-size-fits-all therapies. By focusing on FGFR2 mutations, pemigatinib targets a key vulnerability in certain cholangiocarcinoma cells, offering a more individualized and potentially effective treatment option. This is especially meaningful for a cancer as challenging as cholangiocarcinoma, where few effective treatments exist, and where traditional options often come with high toxicity and limited success.

In conclusion, Dr. Saverno and her colleagues’ research provides insights on the real-world treatment patterns, FGFR2 testing patterns, and effectiveness of pemigatinib for cholangiocarcinoma when used in everyday practice. The results highlight both the drug’s potential and the critical role of genetic testing in identifying the right patients for this targeted therapy. As more studies explore real-world applications of targeted treatments, the hope is that patients with cancers such as cholangiocarcinoma will have more effective, personalized options available, giving them a better chance at managing their disease and enhancing their quality of life. 

Risk factor-based methods have long been the standard in cardiology. These models evaluate a set of variables in a patient’s history and condition, using statistical relationships to estimate risk. For example, if a person with HCM has had fainting spells, a substantial increase in heart size or has a family history of sudden death, these factors contribute to a higher “risk score.” Based on these scores, doctors make decisions on treatments, including whether to implant a defibrillator.

However, Dr Saumarez and colleagues highlight a critical issue: risk factor methods operate on associations rather than causation. They don’t measure the actual conditions in the heart that cause arrhythmias, and as a result, they often miss many cases where sudden death is likely. According to Dr Saumarez’s analysis, these risk factor methods only predict about 50-60% of sudden death cases. Furthermore, these methods can produce a high false positive rate of 15-30% and if one were to identify 70% of at-risk patients using the same method, about half of the remaining patients would be identified as being at risk, meaning that the majority of patients who are unlikely to experience a dangerous arrhythmia are nevertheless recommended for defibrillator implantation. This not only exposes patients to unnecessary surgery and the potential complications of a defibrillator, but it also increases healthcare costs and patient anxiety.

In contrast to risk factor methods, electrophysiological testing directly examines the electrical activity in the heart that could lead to arrhythmias. One promising technique discussed by Dr Saumarez and his team is called paced electrogram fractionation analysis (or PEFA), which has been evaluated in over 600 patients with a number of diseases. PEFA essentially seeks to mimic the heart’s behaviour during moments of stress, conditions under which dangerous arrhythmias are more likely to arise. It is based on the idea that almost all arrhythmias require regions of slowed activation within the heart to be initiated and maintained. PEFA was developed on the basis that individuals at risk of sudden cardiac death would have demonstrable slowed conduction in their hearts, while low risk patients would not.

Here’s how it works in practice: small electrical impulses are applied to stimulate the heart at specific areas through temporary electrodes, and the responses are recorded at other sites within the heart. In people at high risk of sudden death, these recordings usually reveal signs of “fractionation,” where the heart’s electrical signals become irregular and are, most importantly, delayed. These fractionated signals indicate that the heart muscle tissue is not being activated smoothly, which can create the conditions for a re-entrant arrhythmia. This is a state in which the activation follows an irregular, rapid circular path in the ventricles that leads to ventricular fibrillation, the mechanism of sudden death. By analysing these fragmented signals, PEFA can estimate how likely a person is to experience an arrhythmia.

One of the major findings in Dr Saumarez’s study was that PEFA achieved significantly better predictive accuracy than risk factor methods. While traditional risk factor models typically yield an “area under the curve” (or AUC) of around 0.7, indicating only modest predictive ability, PEFA achieved an AUC of around 0.89. A higher AUC score (close to 1) means that the test is much better at distinguishing between those who will and won’t experience an event. In simpler terms, PEFA was able to detect 90% of sudden death cases with only a 20% false positive rate, a considerable improvement over traditional risk factor methods.

The implications of Dr Saumarez’s findings are profound. If electrophysiological methods such as PEFA become more widely adopted, they could transform the way doctors identify and protect patients at risk of sudden death. Electrophysiology-based assessments would allow doctors to pinpoint arrhythmia risks more precisely, reducing the need for unnecessary defibrillator implants and focusing treatment on those who genuinely need it. For patients, this means a more personalized approach to care, less exposure to the risks and costs of unnecessary surgery, and better peace of mind. It should be borne in mind that implantable cardiac devices (or ICDs) are not benign therapy and have numerous complications associated with their use.

Moreover, focusing on the heart’s actual electrical behaviour could lead to a new generation of treatments. By better understanding the mechanisms behind arrhythmias in HCM, researchers could develop therapies that directly address these electrical disturbances, potentially preventing sudden death in a way that is safer and more effective than current options.

Given the potential benefits of electrophysiology, it may seem surprising that traditional risk factor methods remain dominant, which is mainly due to the lack of an alternative approach.  Electrophysiological testing is more complex, requiring specialized equipment and expertise, and is invasive. However, it carries very little risk for patients and is surprisingly safe. While it is more costly than simply measuring risk factors, this is mitigated by reducing unnecessary, very expensive, ICD implantations.

Dr Saumarez and his colleagues hope to stimulate further discussion and research on this topic, contending that the accuracy benefits of electrophysiology justify its use despite these challenges. Their work underscores the need to evaluate prediction methods not only by their convenience or cost but by their effectiveness in saving lives and reducing ICD implantations, the majority of which never deliver therapy. Moreover, the approach may also have relevance to sudden death caused by other diseases, in shifting the paradigm from assessing risk factors to directly examining the causative physiology to more accurately assess risk. This is emphasised by recent research that has shown that the “gold standard” to determine ICD implantation in post-myocardial infarct patients, a reduced Left Ventricular Ejection Fraction, has no predictive capacity whatsoever.

In the future, we may see a shift towards more widespread adoption of electrophysiological methods. Dr Saumarez’s research opens up exciting possibilities for improving the accuracy of sudden death prediction in HCM and potentially in other heart conditions. While non-electrophysiological methods have helped many patients, the insights provided by direct cardiac investigation hold the promise of transforming how we predict and prevent sudden cardiac death. For now, the debate continues, but one thing is clear: better understanding and prevention of sudden cardiac death in HCM may soon be within our reach.

The role of the kidney in diabetes is usually thought of in terms of managing complications, such as protecting itself from high blood sugar-mediated damage. However, the work of Prof. Cersosimo and colleagues highlights a different, more active role for the kidney, where it acts to regulate blood glucose levels. This latest study reveals that in addition to filtering blood to remove waste, the kidney can send signals to the liver that affect how much glucose is released into the blood. This kidney-to-liver communication appears to be particularly influential when patients take dapagliflozin, a drug that blocks glucose reabsorption in the kidneys. One critical aspect of this novel finding is that circulating insulin, which has been traditionally viewed as the principal and most potent regulator of blood glucose levels, becomes less important under the blood glucose-lowering action of SGLT-2 inhibitors in diabetes. 

Dapagliflozin belongs to the SGLT-2 inhibitor class of drugs, which help to lower blood sugar by promoting glucose excretion through urine. By inhibiting a specific protein (SGLT-2) in the kidneys, dapagliflozin reduces the reabsorption of glucose back into the bloodstream, resulting in increased glucose loss through urine. This action offers an innovative way to lower blood sugar without relying on insulin, making SGLT-2 inhibitors especially beneficial for patients whose insulin levels are already compromised. Tissue resistance to the metabolic actions of insulin is a hallmark of type 2 diabetes which, in addition to sustaining high blood glucose and facilitating body fat accumulation, promotes vascular stiffness and the formation of vascular plaques early in the process of atherosclerosis.  

While SGLT-2 inhibitors such as dapagliflozin help to control blood sugar through glucose excretion, in their recent study, Cersosimo and colleagues have found that the body has a natural way of responding to this loss by increasing endogenous glucose production, where the liver produces additional glucose to compensate for what has been lost. This adaptive response is crucial since it prevents the development of life-threatening drops in blood sugar levels, which could lead to seizures, coma and death. As a result, it also reduces the therapeutic effectiveness of dapagliflozin because the liver’s glucose production partially offsets the glucose-lowering effects of the drug.

In order to test whether the stimulation of insulin secretion would magnify the blood glucose-lowering effects of dapagliflozin, Cersosimo and colleagues utilized exenatide, a GLP-1 receptor agonist that helps the body to secrete insulin. When used in combination with dapagliflozin, exenatide seemed to moderate the liver’s compensatory response, thereby helping the combination to achieve a more stable and effective reduction in blood sugar levels. Therefore, SGLT-2 inhibitors combined with GLP-1 receptor agonists, such as exenatide, provide more efficient blood glucose lowering than each drug used alone. This is of interest because under these circumstances the kidney becomes the main “glucose regulator”, overpowering the action of the exenatide-stimulated hormone insulin, and very dangerously low blood sugar levels were never observed.  

Cersosimo’s research has provided evidence for this novel mechanism of glucose regulation, which links the kidneys’ actions to glucose production in the liver. This discovery came from observing the impact of dapagliflozin’s glucose excretion effect on endogenous glucose production, especially when exenatide was added to the treatment. To achieve this, the team conducted a four-month trial with 75 patients with type 2 diabetes who were split into three groups: one group received dapagliflozin, another received exenatide, and the third received a combination of both drugs.

It was through this experiment that the researchers discovered that dapagliflozin disrupts the kidney/liver balance by triggering the kidney to excrete glucose, which signals the liver to continue producing glucose, even when it’s not needed. Adding exenatide helped to partially interrupt this kidney-to-liver signalling, effectively preventing the liver from overproducing glucose in response to dapagliflozin, yet maintaining the intended blood glucose-lowering effects of dapagliflozin.

This newly discovered insight into a kidney-to-liver axis could help to reshape diabetes treatments. By understanding how the kidney and liver communicate to control glucose levels, scientists can design therapies that better leverage this pathway to manage blood sugar. For patients, this could mean treatments that are not only more effective but also potentially more personalized, targeting specific physiological mechanisms that cause elevated blood sugar.

Beyond these physiological insights, this study reinforces the importance of SGLT-2 inhibitors such as dapagliflozin in modern diabetes care. Not only do these drugs provide a novel means of lowering blood sugar, but they also offer significant cardio-renal protection—a major benefit for people with type 2 diabetes, who are at higher risk for heart disease and kidney issues.

Cardiovascular and renal complications are leading concerns in diabetes, and the ability of SGLT-2 inhibitors to help reduce these risks makes them an essential choice in the management of patients with diabetes. SGLT-2 inhibitors can reduce the risk of major cardiovascular events (such as heart attack and stroke) and slow the progression of kidney disease. These safety benefits add substantial value, positioning SGLT-2 inhibitors as a cornerstone of diabetes therapy for patients with or at risk for cardiovascular and renal complications.

The combination of dapagliflozin with exenatide not only resulted in better blood sugar control but also led to sustained improvements in HbA1c (which is a long-term marker of blood sugar levels) and promoted weight loss, an additional benefit in managing type 2 diabetes. HbA1c reductions are crucial, as maintaining a lower HbA1c value over time reduces the risk of complications such as nerve damage, vision issues, and heart problems. The weight loss associated with this combination therapy may also enhance insulin sensitivity, further aiding blood sugar control. In this regard, the novel observation of Cersosimo and colleagues that the kidney, not the hormone insulin, becomes a central player in glucose regulation in diabetes patients treated with SGLT-2 inhibitors, which reduces tissue resistance to the actions of insulin and contributes to enhance insulin sensitivity.

The study shines a light on a promising future for diabetes care, where therapies are not only safe and effective but also address specific mechanisms of glucose regulation. The discovery of a kidney-to-liver signalling pathway opens up exciting new possibilities, both for understanding the body’s glucose regulation and for developing more targeted treatments with specific prevention strategies.

Following a series of observational studies and clinical trials and, based on this particular landmark experiment, Cersosimo and colleagues have contributed significantly to our understanding of glucose regulation in diabetes, uncovering a novel renal-hepatic axis and demonstrating the power of SGLT-2 inhibitors as safe and effective medications. The combination of SGLT-2 inhibitors plus GLP-1 receptor analogues provides a unique approach that taps into the body’s glucose control mechanisms, offering new hope for managing type 2 diabetes. By paving the way for treatments that more completely address the underlying physiology of glucose regulation, this research inaugurates an era where diabetes care is more effective, safe, more protective, and more precisely tailored to each patient’s needs.  The results of this study further contribute to the pursuit of improving the lives of patients with diabetes and prolonging their survival.

The LiverRisk score has been developed by the LiverScreen Consortium, a group of international researchers dedicated to early detection and management of liver disease. Funded by the European Commission, the consortium’s goal is to reduce the global burden of liver disease by developing innovative and accessible screening methods that can be applied on a large scale.

The score was created as part of a major multicohort study involving participants from several countries, including Denmark, Spain, Germany, France, Hong Kong, the Netherlands and the United Kingdom. The participants did not have diagnosed liver disease, and underwent liver stiffness measurements using a technique called transient elastography. Liver stiffness is a key indicator of fibrosis, a process which involves the buildup of liver scar tissue caused by chronic liver injury. As fibrosis gets worse, the liver tissue becomes stiffer, eventually leading to cirrhosis.

The LiverRisk score accounts for eight factors: age, sex, a platelet count, fasting glucose levels, cholesterol levels, and the levels of three liver enzymes (aspartate aminotransferase, alanine aminotransferase, gamma-glutamyltransferase). These health parameters are commonly tested in routine medical exams. By combining these factors, the LiverRisk score predicts a person’s risk of developing liver fibrosis and, over time, more severe liver-related outcomes such as cirrhosis, liver cancer, and liver-related death.

This score is particularly valuable because it categorizes individuals into four risk groups: minimal risk, low risk, medium risk, and high risk. This helps healthcare providers to easily identify which patients are most in need of follow-up, preventive care, or lifestyle changes.

Liver diseases are often called “silent killers” because they develop slowly and show few or no symptoms until they reach an advanced stage. Many people with liver fibrosis or even early cirrhosis may feel fine and only discover their condition when it has progressed to the point where liver function is seriously impaired. At this stage, the only curative option may be a liver transplant, which is a major procedure with limited donor availability.

That’s where the LiverRisk score comes in. It aims to catch liver disease early, when it can still be managed with lifestyle changes or medical interventions, potentially preventing the progression to cirrhosis or liver cancer and the need for a liver transplant. For example, people with metabolic associated steatotic liver disease can often improve their liver health by losing weight, exercising, and managing conditions such as diabetes. Similarly, reducing alcohol consumption can significantly improve liver disease in people with alcohol-related liver disease. However, these interventions are most effective when the disease is caught early—before irreversible damage occurs.

The LiverScreen Consortium’s study validated the LiverRisk score in large populations, showing that it effectively identifies individuals at risk for serious liver conditions. More than 14,000 people participated in the initial study cohorts, and the LiverRisk score was further tested in additional groups, including over 400,000 participants from the UK Biobank study. The results were promising.

The LiverRisk score was found to be highly accurate in predicting liver fibrosis and future liver-related outcomes. For instance, in predicting liver-related death, the score performed better than existing tools such as the fibrosis-4 (FIB-4) index, which is commonly used. The LiverRisk score had an area under the curve of 0.90, meaning that it was very good at distinguishing between those at high risk and those at lower risk, compared to 0.84 for the FIB-4 index.

Over a follow-up period of more than 12 years, those in the high-risk group were shown to have a high risk of liver-related death compared with those in the minimal-risk group. This demonstrates the score’s ability to clearly differentiate between those who need urgent attention and those at lower risk.

In addition to liver-related death, the LiverRisk score was also effective at predicting other outcomes, including hospitalization due to liver disease and the development of liver cancer. For instance, the study found that participants in the high-risk group had a much higher chance of being hospitalized for liver-related issues than those in the minimal-risk group.

One of the LiverRisk score’s greatest strengths is its simplicity and accessibility. Unlike costly or invasive tests such as liver biopsies, the LiverRisk score can be calculated using routine blood tests. This means that general practitioners and healthcare providers can use it widely, especially in primary care settings, where the early identification of liver disease could make the biggest difference.

Integrating the LiverRisk score into routine health checkups, especially for individuals with known risk factors such as obesity or diabetes, could allow doctors to identify at-risk individuals much earlier. The score can serve as a wake-up call, encouraging patients to adopt healthier lifestyles or seek specialized care before it’s too late.

Moreover, the LiverRisk score has the potential to become a useful tool for population-wide screening. In regions with high rates of liver disease, such as those with widespread alcohol use or rising rates of obesity, this tool could help prioritize resources by identifying who is most at risk and needs intervention.

This research represents a significant step forward in public health, as liver disease remains one of the leading causes of death worldwide. While cirrhosis is often viewed as an inevitable consequence of years of silent liver damage, the LiverScreen Consortium’s work suggests that many cases could be prevented with early detection and timely intervention.