As reviewed by Peters and Sacks[5] chronic or progressive leishmaniasis has been associated by the parasite’s ability to evade macrophage defense mechanism such as killing by oxygen-derived free radicals, to produce defects in the induction and expression of cell-mediated immune mechanisms such as suboptimal T-cell receptor (TCR) signaling and the inability of Leishmania-infected macrophages to produce IL-12 as the main inducer of IFN-y and CD4+ T cell Th1 differentiation resulting in defected cellular immune response. This evidence concerns the gene CD4 and leishmaniasis.