Given the profoundly altered pathogenesis of MHV68 infection in mouse models of global type I or type II IFN deficiency and the critical effector role of STAT1 downstream of all IFN receptors, we sought to generate a mouse model with all classical IFN signaling specifically attenuated in B cells. This evidence concerns the gene STAT1 and hyperinsulinemic hypoglycemia, familial, 4.