RICTOR and infection: Taken together these findings and the results from Rictor knockout cells that activate mTORC1 to the same extent as Rictor wild-type cells in the presence of p-AKT(308) but in the absence of p-AKT(S473), these findings point to the AKT T308 phosphorylation site as important to stimulate mTORC1 activity during infection (Fig 1B–1E).