In glioma cells, we demonstrate that an increase in endosomal PtdIns(3,4)P2 in response to PDGF–BB is a prerequisite for AKT phosphorylation at Ser473 but not at Thr308 using a drug-inducible heterodimerization system and for targeting mTORC2 into endosomes via mSIN, which contains an RBD-PH domain, to specifically bind PtdIns(3,4)P2. The gene discussed is AKT1; the disease is glioma.