Although it has been proposed that EPO reduction of cardiac ischemia/reperfusion injury is mediated by eNOS activity via NO secretion by cardiomyocytes [94], EPO treatment in mice with endogenous EpoR expression restricted largely to hematopoietic and endothelial cells exhibited stimulated eNOS activation in endothelial cells and reduced ischemic reperfusion injury similar to wild type control mice [87]. Here, EPO is linked to myocardial ischemia.