PNPLA3 and steatosis: A model that has been proposed that is consistent with the neomorph hypothesis is that PNPLA3-I148M sequesters CGI-58/ABHD5, a cofactor for the triglyceride hydrolase ATGL/PNPLA2, impairing triglyceride hydrolysis on cytosolic lipid droplets (LDs) and thereby driving steatosis (26, 27).