1, 2, 4, 5 Activation of mTOR and AKT increases phosphorylation of PRAS40 and causes it to dissociate from Raptor, which subsequently relieves the inhibitory constraint on mTORC1-mediated phosphorylation of 4E-BP1 and p70S6K.6 PRAS40-mediated inhibition of mTORC1 is well-documented; however, there are several reports indicating that PRAS40 may have additional functions in cancer cells. This evidence concerns the gene AKT1 and cancer.