Previous animal studies suggest that different strains of leishmaniasis induce different host immune responses, and that a Th1 response results in resolution of infection whereas a Th2 response results in development of severe disease.[22] The Th1 response produces INF-γ, which correlates with resistance; whereas the Th2 response produces IL-4 and correlates to susceptibility to infection.[69] In humans, IL-4, a component of the Th2 response, is also associated with disease development.[70, 71]. The gene discussed is IL4; the disease is leishmaniasis.