Since the disease in the GFAP-Cre STAT1f/f mice resembles that in chronically infected mice with severe immune deficiencies (i.e., treated with neutralizing antibodies specific for IFN-γ or depleted of both CD4+ and CD8+ T cells), it seems unlikely that the relatively modest changes in effector function would be sufficient to explain the high parasite burden in the GFAP-Cre STAT1f/f mice. The gene discussed is IFNG; the disease is Immunodeficiency.