Large‐scale follow‐up studies are clearly warranted to further substantiate the significant prevalence of inactivating TAL variations in the general population as well as its role in predisposition to liver diseases, such as non‐alcoholic steatohepatitis, cirrhosis, HCC, and susceptibility to APAP‐induced liver failure. This evidence concerns the gene TALDO1 and metabolic dysfunction-associated steatohepatitis.