The fact that concomitant infections with helminths enhance malaria morbidity by driving the differentiation of Th2 cells and the prevalence of the type 2 cytokines such as IL-4, and IL-13 [6], and that a potent IFN-γ response at the early phase of infection correlates with protection, suggest a protective role for Th1 responses in human malaria [4], [7]. The gene discussed is IL4; the disease is infection.