The PNPLA3 I148M variant is also associated with increased risk of fibrosis progression and HCC in cirrhosis from hepatitis C and alcoholic liver disease independent of steatosis[35–37], suggesting a potential direct contribution of the variant to fibrogenesis and carcinogenesis that are unrelated to intrahepatic triglyceride accumulation[38]. This evidence concerns the gene PNPLA3 and hepatocellular carcinoma.