Thereby AKT could relieve mTORC1 inhibition by phosphorylating PRAS40.16 As an inhibitor of mTOR, PRAS40 prevents mesangial cell and myocardium hypertrophy,17, 18 reduces H293E cell size and growth2 and improves insulin sensitivity.9, 19 Inactivating frameshift mutation of AKT1S1 has been detected in colorectal cancers.20 But depletion of PRAS40 has been found to decrease cell proliferation in nearly all the studies of PRAS40 in cancer cell models excluding colon cancer.10, 11 It remains unclear for the detailed mechanism of PRAS40 in cell prosurvival. The gene discussed is MTOR; the disease is cancer.