In early stages of active infection, Th1 cellular immune responses are protective, as interferon gamma (IFNγ) and interleukin 12 (IL-12) induce macrophage activation, allowing bacterial growth control; nevertheless, during late active disease, extensive inflammation leads to a shift toward a Th-2 immune response in which IL-4, IL-10, and transforming growth factor-β (TGF-β) induce a local anti-inflammatory and immunosuppressive milieu resulting in poor containment of infection and progression of tissue damage, necrosis, and fibrosis, driving host to death (6). The gene discussed is IFNG; the disease is infection.