For many years non-alcoholic fatty liver disease (NAFLD) and alcohol-related liver disease (ALD) have been considered as two biologically and clinically distinct conditions. According to the newly introduced nomenclature of steatotic liver disease (SLD), 1 patients with moderate excessive alcohol consumption and metabolic risk factors who are diagnosed with SLD will be referred to as having MetALD. There is rapid development underway for the treatment for patients with metabolic dysfunctionassociated steatotic liver disease (MASLD) and metabolic dysfunction-associated steatohepatitis (MASH), which had been known as non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH), respectively. Several drugs for MASH are in phase 2 and phase 3 trials. Some medications will probably reach the market soon, finally making a pharmacological treatment available for one of the world’s most prevalent liver diseases. However, these developments also carry an important dilemma for all stakeholders in the field of hepatology—what should be the approach to alcohol intake in the management of SLD? First, when a patient is diagnosed with SLD, the subclassification into MASLD, MASH, or MetALD depends on patient’s self-reported alcohol intake, which is often inaccurate. 2 Therefore, should the decision to offer pharmacological treatment for MASH be based solely on patients’ self-reported alcohol consumption? Moreover, the potential influence of alcohol consumption on the participants enrolled in the MASH trials is worth considering. Some promising candidate drugs for MASH, such as GLP-1 receptor agonists and FGF21 analogues, might reduce patient alcohol use. 3 Could beneficial drug effects seen in the MASH trials also be associated with reduced alcohol consumption? The diagnostic challenge of distinguishing between MASLD, MetALD, and ALD is further complicated by the fact that many patients who consume alcohol also have metabolic risk factors. 4 Although excessive alcohol use is presumed to be the most important risk factor for liver disease, 5 alcohol and metabolic risk factors act synergistically on the overall risk of developing severe liver disease (figure). 6

We must acknowledge that MetALD and ALD are the leading causes of liver-related morbidity and mortality. 7 Robust diagnostic and prognostic biomarkers have been developed over the past decade allowing for early diagnosis of MetALD and ALD. 8 The current focus and capability to identify liver disease early7 have led to an increasing demand for treatments for MetALD and ALD. However, unlike MASH, there are few drugs in the development pipeline for MetALD and ALD. Although this issue might be complex and multifactorial, one reason contributing to the scarcity of treatments is that patients with MetALD and ALD are stigmatised. Among health-care professionals, researchers, and the pharmaceutical industry there has been a perception that MetALD and ALD result from self-inflicted behaviour, that individuals who are affected could simply stop drinking alcohol, and that developing