To conclude, we have demonstrated the direct binding by miR-122 to the 3′-UTR of the human AKT3 and the overexpression miR-122 in the HBV-altered HCC cell lines which is efficient to reduce AKT3, at transcript as well as the protein level in order to obstruct the cell relocation, prompting the apoptosis and hindering the cell growth as well as the tumor growth in the mice. This evidence concerns the gene AKT3 and hepatocellular carcinoma.