Although STAT1 is a critical component of both type I and II IFN-mediated antiviral responses, STAT1-deficient mice are more resistant to infection with Sindbis virus or murine cytomegalovirus (MCMV) than type I and II IFN receptor-deficient (AG129) mice [20], suggesting that IFN receptors also signal through STAT1-independent mechanisms [21]–[23]. The gene discussed is IFNA1; the disease is infection.