The colonization of the heart tissue by CCR5+ CD8+ T-cells (and also CCR5+ macrophages) may contribute to create a CCL3-enriched milieu, and critically auto-sustain the infiltration of the heart tissue by these cell, as supported by the partial abrogation of the acute (13) and chronic T. cruzi infection-elicited myocarditis (15, 16) by the CCR1/CCR5 antagonist Met-RANTES (23). This evidence concerns the gene CCL3 and myocarditis.