The role for IFN-γ is not as well established in the pathogenesis of myocardial disease; however, transgenic mice that constitutively express IFN-γ in liver tissue driven by the liver specific promoter of human serum amyloid P component (SAP) gene were recently shown to develop chronic active myocarditis and cardiomyopathy [48]. This evidence concerns the gene IFNG and myocarditis.