In cutaneous leishmaniasis, the development of a non-healing course of infection has been linked to an immunosuppressive profile, with increased arginase 1 activity [45], a cytosolic enzyme that favors parasites’ antioxidant metabolism and that, at the same time, competes with iNOS for the common substrate L-arginine, decreasing NO production [46,47]. The gene discussed is NOS2; the disease is infection.