IL-12 mediated Th1 responses had been believed to increase CVB3-induced myocarditis in susceptible BALB/c mice, but results showed that IL-12 deiciency did not prevent the development of acute myocarditis[12], and mice lacking IFN-γ were highly susceptible to EAM [5,6], which means that these cells do not sustain or play decisive roles in myocardial autoimmune injury. The gene discussed is IFNG; the disease is acute myocarditis.