Alcohol-related liver disease (ALD) is a major health concern and recent studies have reported nearly 1 million alcohol-related deaths from 1999 to 2017 in the United States.¹ ALD is a spectrum of conditions that ranges from early steatosis or fatty liver to inflammation or alcoholic steatohepatitis progressing to fibrosis and cirrhosis. Approximately 8%–20% of alcoholic steatohepatitis patients develop cirrhosis and, in some, alcoholic steatohepatitis can present in the form of acute-on-chronic liver failure, termed alcoholic hepatitis, owing to excessive drinking episodes. Corticosteroids are the first line of therapy for ALD, however, only marginal short-term survival benefit in patients with severe alcoholic hepatitis has been reported.² Studies from the National Institute on Alcohol Abuse and Alcoholism consortia have focused on preclinical or early clinical testing of drugs classified on the basis of pathogenic mechanisms such as targeting the gut–liver axis, anti-inflammatory agents, antioxidants, and drugs that promotes liver regeneration.³ Despite several efforts, the treatment for alcoholic hepatitis remains suboptimal and there is an urgent need to develop new, safe, and effective therapies. Uncovering new targets directly involved in regulatory processes that influence gene expression and cellular phenotype could be an attractive strategy.