Studies have shown that overexpression of VEGF-B in myocardium could promote neovascularization directly from the ventricle, maintain the connection with coronary vessels in subendocardial myocardium, accelerate the proliferation of subendocardial myocardial endothelium, and rescue the structure and function of myocardial tissue after MI (75). This evidence concerns the gene VEGFB and myocardial infarction.