AKT1 and endothelial dysfunction: Furthermore, we uncovered that Rb1 activated AKT phosphorylation‐mediated angiogenesis through binding to VEGFR2, which promoted endothelial tube formation and nitric oxide (NO) release in human umbilical vein endothelial cells (HUVECs) and then relieved the endothelial dysfunction induced by hypoxia‐reoxygenation (H/R).