Despite their robust anti-parasitic effects, IFN-γ and TH1 T cells may also promote disease severity, as high levels of circulating IFN-γ correlate with malaria pathology in humans and mice [15,55,56]. In murine models, lack of IFN-γ protects against ECM and reduces production of pro-inflammatory cytokines [53]. The gene discussed is IFNG; the disease is malaria.