In mouse models, the pathophysiology of CVB3‐activated myocarditis involves several Inflammatory processes (a) up‐regulation of CyPA and its extracellular receptor CD147, (b) CyPA is crucial for the recruitment of macrophages and T cells along with the defence against the virus during the early stages of CVB3 infection, and (c) ability of CsA analog, NIM811, to inhibit cyclophilin and provides protection against myocardial fibrosis, can be measured based on the collagen tissues in the chronic myocarditis during CVB3 infection. The gene discussed is BSG; the disease is myocarditis.