Similarly, by using IFN-α/β receptor 1−/− and Batf3−/− mice transplanted with B16 melanoma, Fuertes et al. (49) reported that endogenous IFN-I, produced shortly after tumor challenge, was essential for intratumoral accumulation of CD8α DC and for induction of tumor Ag-specific T-cell priming and tumor rejection via CD8α DC stimulation. The gene discussed is CD8A; the disease is neoplasm.