Apocynin treatment caused a decrease in ROS release due to a decrease in the proliferation of immune cells (CD68 macrophages, neutrophils, Ly-6G/Gr-1, CD4 and CD8 T lymphocytes), decreased the proinflammatory cytokine production during the acute phase of infection, and consequently controlled the hypertrophy, myocarditis, and cardiac fibrosis, avoiding excess ROS release due the apocynin administration [51]. This evidence concerns the gene CD68 and myocarditis.