It is known that the activation of AKT mediates the phosphorylation of GSK3β, resulting in the nuclear translocation of β-catenin from the cytoplasm and increased transcription, leading to the regulation of downstream cyclin D1, c-Myc, and CD44 protein expression, which ultimately inhibits HCC tumor growth [31]. This evidence concerns the gene AKT1 and hepatocellular carcinoma.