Although PNPLA3 is the most studied gene susceptible to NAFLD, a functional study using knockout mice did not find any abnormal metabolic phenotype.13, 14 Moreover, liver‐specific PNPLA3 I148M overexpression15 and I148M point mutation knock‐in mice16 exhibited significant susceptibility to liver fat deposition induced by a high‐sucrose diet but did not show evidence of the promotion of NAFLD progression, such as nonalcoholic steatohepatitis (NASH) and hepatic fibrosis. This evidence concerns the gene PNPLA3 and metabolic dysfunction-associated steatohepatitis.