Also, in P. berghei ANKA-infected mice, which produce low levels of early type I IFN response but produce a significant amount at a somewhat later stage (4 days postinfection), deficiency in IFNαR or treatment with anti-IFNαR1 antibody resulted in increased IFN-γ production, increased number of IFN-γ-positive NK and CD4+ T cells in the spleen, and significantly decreased parasitemia and protection from cerebral malaria (175, 176). The gene discussed is IFNAR1; the disease is cerebral malaria.