Seminal work from the Biron laboratory has shown in the murine LCMV infection model that Stat4 is required for innate IFNγ production by natural killer cells but also that viral infection induces a switch in CD8 + T cells from a Stat1-dependent, anti-proliferative effect to a Stat4-dependent, IFNγ production in response to IFNα (62, 70, 71). The gene discussed is CD8A; the disease is viral infectious disease.