Although IFN-γ is dispensable for protection against influenza infection, SOCS1-deficient CD8+ T cells from SOCS1−/− IFN-γ−/− mice were sufficient to improve antiviral immunity and, furthermore, SOCS1-enhanced lung injury occurred after IFN-γ production was diminished in WT mice, we cannot exclude the possibility that these detrimental effects of SOCS1 were significant only in the absence of T cell IFN-γ production. The gene discussed is SOCS1; the disease is influenza.