We investigated how FAT/CD36 functions physiologically during the progression of liver diseases, which is in line with the traditional theory of liver disease development: “non-alcoholic fatty liver disease (NAFLD) – non-viral hepatitis – liver fibrosis – hepatocellular carcinoma.” qPCR and Western blot analyses confirmed that fraxin modulates FAT/CD36 expression at both the mRNA and protein levels. This evidence concerns the gene CD36 and viral hepatitis.