Collectively, these pieces of evidence reinforce that Tr1 cells, locally induced by Ebi3, protected the host from the inflammation caused by IFN-γ, thus highlighting a novel mechanism employed by Ebi3 to dampen T. cruzi-induced myocarditis via accumulation of Tr1 cells in the heart and suppression of IFN-γ. Here, IFNG is linked to myocarditis.