However, in contrast to the relative increase in IL-17–producing cells under Th17 conditions, our novel discovery is that IFN-γ–producing T cells among Egr2 and 3–deficient T cells were profoundly increased in all Th conditions, as well as in effector T cells generated in response to viral infection, demonstrating a distinct and fundamental role for Egr2 and 3 in the control of T-bet–mediated IFN-γ production in effector T cells. Here, IFNG is linked to viral infectious disease.