In our previous investigation, we demonstrated that loss of Akt2, the major AKT isoform in the liver, is sufficient to completely prevent HCC development induced by E545K/c-Met or H1047R/c-Met in mice, suggesting that AKT2, rather than SGK3, is the major and critical downstream effector of activated PIK3CA mutants required for HCC formation. This evidence concerns the gene PIK3CA and hepatocellular carcinoma.