AKT1 and myocardial infarction: On the same line, Lu and coworkers reported that the overexpression of miR-130a promotes endothelial cell proliferation and migration by increasing Akt phosphorylation and inhibiting PTEN (30); the same group also demonstrated that the activation of PI3K/Akt signaling enhances angiogenesis and decreases the progression of MI and fibrosis, attenuating myocardial dysfunction and reducing the risk of cardiac rupture post-MI (30).