In our Cx3cr1‐Rheb1Δ/Δ model, T‐cell effector profiles were stimulated, as shown by the increased proliferation and expression of cytotoxic factors such as IFNγ, granzyme b and perforin, in keeping with a scenario where mTOR significantly contributes to TAM‐mediated T‐cell dysfunction in GBM. The gene discussed is PRF1; the disease is glioblastoma.