Young mice rejected the OVA-expressing tumour even when IFN-γ-deficient OT-II was transferred, because IFN-γ deficiency in the transferred OT-II cells could be counterbalanced by abundant IFN-γ-producing endogenous WT CD4+ T cells in young mice, which might be sufficient to mount antitumour immunity. The gene discussed is IFNG; the disease is neoplasm.