To elucidate the molecular mechanisms by which SH2B1 modulates NSCLC cell proliferation, we investigated the effects of knock-down and over-express SH2B1 on the phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of Rapamycin (mTOR) signaling, which is an important regulator of cell proliferation and frequently aberrantly activated in human cancers [12, 13]. The gene discussed is MTOR; the disease is cancer.