Targets PIK3R2 and SPRED1 expression, resulting in elevated activity of the PI3K/Akt signal and improved angiogenesis, left ventricle function after MI, and alleviated apoptosis of both endothelial cells and cardiomyocytes [278,279,280,281,282,283,284]. This evidence concerns the gene AKT1 and myocardial infarction.