This is likely related to the capacity of IFNγ and TNF to evoke “bystander” activity on tumor cells not directly targeted by the CAR T cells33, modulation of other immune cells within the tumor microenvironment, and/or its propensity to modulate the tumor stroma and inhibit neovascularization as previously observed in the context of A2AR-deficient T cells7. The gene discussed is IFNG; the disease is neoplasm.