To address this question, and to avoid pitfalls associated with altered immune system development or dysregulated hematopoiesis in ifnar1-/- mice [54, 55], we employed transient blockade of type I IFN responses and chimeric/genetic approaches to evaluate CD4 T cell intrinsic and extrinsic roles for type I IFN signaling during experimental malaria. The gene discussed is IFNAR1; the disease is malaria.