Previous evidence has suggested that PARP may be excessively activated by reactive oxygen and nitrogen species in cardiomyocytes and endothelial cells, during myocardial ischemia/reperfusion injury, various forms of heart failure or cardiomyopathies, circulatory shock, cardiovascular aging, diabetic complications, myocardial hypertrophy, atherosclerosis, and vascular remodeling following injury (21). The gene discussed is PARP1; the disease is cardiac hypertrophy.