In fact, in visceral leishmaniasis, the acquisition of intrahepatic resistance to the parasite is a consequence of the tissue expression of a protective T cell response that promotes the attraction of competent cells to potentiate the anti-microbial activity of infected Kupffer cells by inducing the production of reactive oxygen and nitrogen intermediates as well as the pro-inflammatory cytokines IFN-γ and TNF-α, which play a critical role in liver granuloma formation and control of parasite colonization [22]. The gene discussed is IFNG; the disease is visceral leishmaniasis.