The importance of CGI-58 in hepatic steatosis, NASH, and fibrosis has been clarified through studies on CGI-58 knockout mice and the CGI-58 mutation population.18,41 Furthermore, the deficiency of liver ATGL caused hepatic steatosis, but not NASH or fibrosis,17,42 suggesting that CGI-58 could regulate hepatic inflammation and fibrosis through an ATGL-independent mechanism.43 However, the mechanism of CGI-58 in regulating NASH and fibrosis is still unclear. This evidence concerns the gene PNPLA2 and metabolic dysfunction-associated steatohepatitis.