When tumor cells are killed by T cells in the TIME, increased extracellular potassium is released from necrotic cells into the tumor interstitial fluid, in turn metabolically reprogramming T cells to exhibit stem‐like qualities and self‐renewal but impairing T‐cell receptor‐mediated Akt–mTOR phosphorylation and effector function [98, 99]. The gene discussed is MTOR; the disease is neoplasm.