Several mechanisms are implicated, including the inactivating mutation of PTEN (116, 117), the mutation/amplification of PI3K-AKT (118), the hyperactivation of PI3K-AKT signaling pathway by growth factors (e.g., insulin, PDGF, VEGF, HER-2, IGF-I), the overexpression of mTORC1 targets (i.e., S6K1, 4BP1, eIF4E), or the loss of tumor suppressors (e.g., PTEN, LKB1, or TSC). Here, AKT1 is linked to neoplasm.