Indeed, p.I148M overexpression raised hepatic TG concentrations in wt, but not in Cgi-58 knock-out (KO) mice, indicating that the PNPLA3 mutation may prompt hepatic steatosis, hindering ATGL/PNPLA2 activity on LDs in a CGI-58-dependent manner. Here, PNPLA3 is linked to fatty liver disease.