Previous reports by our laboratory and others have shown that T. gondii–infected Tbx21−/− mice retain the capacity to generate NK- and T cell–derived IFN-γ, and thus it is unlikely that T-bet–deficient animals with or without IL-12 treatment succumbed to infection due to the absence of IFN-γ (7, 16, 17). This evidence concerns the gene IFNG and infection.