Our previous studies using mouse models of liver disease induced by a choline-deficient, L-amino acid-defined diet or by diethylnitrosamine administration elucidated that CYGB deficiency accelerated oxidative stress, liver inflammation, and fibrosis, and the development of hepatocellular carcinoma (HCC), accompanied by the activation of HSC (Thuy et al, 2015; Thuy et al, 2011). This evidence concerns the gene CYGB and hepatocellular carcinoma.