We have subsequently shown that long-term cardiac-specific overexpression of resistin in vivo using adeno-associated virus serotype 9 significantly decreased left ventricular contractility and induced a complex phenotype of oxidative stress, fibrosis, apoptosis and myocardial remodeling in normal rats29, very much resembling a diabetic cardiomyopathy phenotype. The gene discussed is RETN; the disease is diabetic cardiomyopathy.