Interestingly, the interaction between Akt and GSK-3β builds a bridge between the PI3K-Akt and Wnt signaling pathways to make it possible to regulate oncogenesis synergistically: Akt can not only recognize the accumulation of phosphatidylinositol 3,4,5-trisphosphate (PIP3) provoked by PI3K to stimulate a downstream of the classic PI3K-Akt signal [29], but also the accumulation of phosphorylate GSK-3β at the Ser9 site [30], further regulating β-catenin localization in Wnt signals and therefore affecting other inhibitors downstream, including slug and MMP2, to influence tumor growth [31,32]. Here, AKT1 is linked to neoplasm.