Inhibits angiogenic function of CMECs by decreasing the PI3K/Akt signal activity [319], regulates cardiac hypertrophy by modulating the p-Akt activation [320], and mediates cardiac fibrosis after MI targeting RASA1 expression, which promotes MEK1/2, ERK1/2 and AKT phosphorylation [321]. This evidence concerns the gene AKT1 and fibrosis.