In VL (both in murine and human), resolution of infection depends on the induction of cellular immunity along with the production of pro-inflammatory, or Th1, cytokines.8–15 Specifically, production of interleukin12 (IL12) by antigen-presenting cells and interferon gamma (IFNγ) by T cells are crucial for controlling the parasite growth and development of host-protective immunity.8,16 In contrast, susceptibility to VL is correlated with the presence of a Th2-type anti-inflammatory response.17L. The gene discussed is IFNG; the disease is infection.