The latter protein was investigated since: (1) NDRG1 overexpression increases PTEN protein levels in prostate and pancreatic cancer cells (12, 83); (2) PTEN positively upregulates NDRG1 protein expression in prostate and breast cancer cells (84); and (3) PTEN is a tumor suppressor that dephosphorylates phosphatidylinositol-3,4,5-trisphosphate (PIP3) to phosphatidylinositol-4,5-bisphosphate (PI(4,5)P2), inhibiting the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) pathway (85, 86). Here, AKT1 is linked to breast cancer.