Several early studies suggested that resistance or susceptibility to infection caused by L. major was controlled by the behavior of different subpopulations of helper T cells (33, 34), because the amount of IL-4 produced by T helper 2 (Th2) cells appeared to correlate with progression of leishmaniasis, whereas activation of IFNγ-producing Th1 lymphocytes, which promotes the production of nitric oxide in phagocytes at the site of infection (35), has been associated with resolution of the disease. The gene discussed is IL4; the disease is infection.