Our previous studies demonstrated that the down-regulation of NDRG2 induced aberrant activation of the PI3K/AKT signaling pathway through the inactivation of PTEN by phosphorylation at its C-terminus, thereby resulting in significantly increased cell proliferation in ATL cells and many other types of cancer cell lines in vitro and tumor incidence in Ndrg2-deficient mice in vivo. This evidence concerns the gene PTEN and neoplasm.