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. The gene discussed is SGK3; the disease is hepatocellular carcinoma.