In the past few years, activation of AKT/GSK3β/β-catenin pathway was reported to be implicated in tumorigenesis of HCC.10 AKT was phosphorylated on Thr308 in the catalytic domain and Ser473 in the C-terminal domain by PDK1 and 2, respectively.11, 12 Then, phosphorylated AKT in turn increased GSK3β phosphorylation at Ser9, which could inhibit β-catenin phosphorylation and degradation by proteasomal pathway.13β-Catenin increased expression levels of a series of downstream oncogenes. This evidence concerns the gene GSK3B and hepatocellular carcinoma.