However, the observation that IL-12-mediated tumor rejection operated in IFN-γ−, IFN-γR−, or perforin-deficient mice suggests that in this model NKp46+LTi do not contribute to the antitumor activity of other innate (NK) or adaptive (CD4+ and CD8+ T) cells in the TME [82]. The gene discussed is CD8A; the disease is neoplasm.