In non-canonical TGF-β signaling, ligand-bound TGF-β receptors activate other signaling pathways, such as p38 and Jun N-terminal kinase (JNK) mitogen-activated protein kinase (MAPK) pathways, phosphoinositide 3-kinase-Akt-mTOR pathway, small GTPase RhoA and Rac/Cdc42 pathways, and Ras-Erk pathway; the activation of these pathways likely enhances tumor growth after canonical TGF-β-Smad signaling is disrupted6,.7 This evidence concerns the gene AKT1 and neoplasm.