(37, 38) demonstrated that T. gondii infection of Rag2−/−γc−/− mice resulted in the appearance of IFN-γ+ cells and the induction of IFN-γ at significantly higher levels than WT mice, suggesting that myeloid cell–derived IFN-γ is sufficient for acute resistance against intracellular pathogen infection. The gene discussed is IFNG; the disease is infection.