We used bioinformatics analysis, paired HCC patient specimens, HBx transgenic (HBx‐Tg) mice, xenograft nude mice, HBV stable replication in the HepG2.2.15 cells, and anti‐HBx antibody intervention to systematically evaluate the biological function of protein kinase B (AKT) dephosphorylation through B56γ in HBx‐associated hepatocarcinogenesis. The gene discussed is AKT1; the disease is hepatocellular carcinoma.