In tune with this, wild-type C57BL/6 mice infected with T. cruzi survived, but IL-10−/− mice with the same genetic background presented a high mortality rate, despite presenting low parasitemia levels and high systemic production of pro-inflammatory cytokines (IFN-γ, IL-12, and TNF-α) during the acute phase of infection [34], [36]. This evidence concerns the gene IFNG and parasitic infectious disease.