In mouse models, NK cells facilitated the accumulation of T-bet+CD4+ T cells in the tumor region (27), promoted the production of effector molecules, TNF-α and IFN-γ, by tumor-infiltrating CD8+ T cells, suppressed the expression of exhaustion marker PD-1 on these CD8+ T cells (28), and promoted the induction of tumor-specific T cell memory (29). The gene discussed is IFNG; the disease is neoplasm.