Resistance to Plasmodium infections has been associated with an early inflammatory Th1-type immune response characterized by IL-12, TNF-α, and IFN-γ production (Langhorne et al., 2004), followed by antiinflammatory Th2 response characterized by IL-4 and IL-10, which is required to control chronic parasitemia and avoid pathologic damage due to exacerbated inflammatory responses (Schofield and Grau, 2005). The gene discussed is IFNG; the disease is parasitic infectious disease.