Given the importance of insulin signaling as a driver of T cell glycolytic activity and proliferation (28, 29) together with the known role of mTORC1 signaling as an inhibitor of insulin signaling (30), these results suggest that the disruption of BsAb-induced mTOR activation may interfere with a negative feedback pathway that constrains insulin-regulated T cell expansion, thus benefitting prolonged T cell activation and target tumor cell killing. Here, INS is linked to neoplasm.