The activation of β-catenin, which was observed in HCC patients with good prognosis [5], was observed in a majority of Myc transgenic mouse model in addition to Ctnnb1 model while it was lowest in models associated with poor prognosis, SV40, Mst1/2 KO, and Sav1 KO models, suggesting β-catenin is a frequent co-activating partner of Myc in hepatocarcinogenesis. This evidence concerns the gene CTNNB1 and hepatocellular carcinoma.