Erythropoietin (EPO) supplementation prevented LV-dilatation and deterioration of cardiac function post-MI, attributed to increased capillary growth as a result of VEGF expression by the myocardium and EPO-induced mobilisation of endothelial progenitor cells (EPCs) from the BM with homing to the cardiac microvasculature [103]. This evidence concerns the gene EPO and myocardial infarction.