First, treatment of mice with recombinant hybrid HuIFNα1/α8, which has activity on murine cells, concurrent with P. yoelii (265 BY) infection decreased early parasitemia, and the authors proposed that this was due to IFNα-dependent inhibition of reticulocyte (immature red blood cell) development, as opposed to direct anti-plasmodium effects (202, 211). The gene discussed is IFNA2; the disease is parasitic infectious disease.