It exerted a strong response with IFN-γ, IL-1β, and IL-12B, resulting in a decrease in parasitaemia and tissue parasitosis, as has been reported by other authors [55,56]; however, the elevated concentration of IL-10 could have several explanations: preventing immune hyperactivity during infection [57], limiting the parasite load, and protecting against fatal myocarditis [58], or improving susceptibility to infection with T. cruzi with a fatal cardiac presentation [59]. The gene discussed is IL1B; the disease is infection.