In breast cancer cells, the anti-proliferative function of the PTEN tumor suppressor protein has been demonstrated to involve the inhibition of AKT-mediated cell cycle activation through both its protein and more canonical lipid phosphatase activities and the function of the CDKN1B cell cycle inhibitor has been shown to be directly inhibited by AKT-dependent phosphorylation [6-9]. This evidence concerns the gene AKT1 and breast carcinoma.