Interestingly, deletion of hepatic MFN2 significantly promotes inflammatory responses, accumulation of triglycerides, fibrosis, and HCC in mouse models of NASH, whereas restoring MFN2 expression using adenovirus in mutant (liver-specific) mice lacking MFN2 observably alleviate disease symptoms of NASH.209. This evidence concerns the gene MFN2 and hepatocellular carcinoma.