AKT1 and cancer: However, inhibition of mTORC1 can lead to RAS-MEK-ERK activation through PI3K-dependent feedback but not mTORC2, AKT or targets of downstream of AKT in human cancer [62], which reveals an alternative signal whereby phosphorylation at Ser259 of Raf by AKT deactivated and inhibited the signal cascade of RAS-MEK-ERK [155] (Fig. 3).