AKT1S1 and cancer: Our data suggest that in cancer cells, AKT and mTORC1 cooperate to maintain phosphorylation of PRAS40, which in turn, relieves PRAS40-inhibitory constraint on mTORC1 activity; the activated mTORC1 supports cap-dependent translation by phosphorylation of 4E-BP1 and promotes cell growth and motility.