In this study, we showed that a global absence of IFN-γ during T. cruzi infection (1) induced similar parasitemia and cytokine and chemokine levels (TNF-α, IL-6, IL-10, MCP-1, and IFN-γ) in WT and IFN-γ(−/−) infected mice in the early stage of infection and (2) delayed the onset of electromechanical remodeling in the LVC and RVC from the mice. This evidence concerns the gene CCL2 and parasitic infectious disease.