It was reported that exogenous Angptl4 protected endothelial barrier integrity by inhibiting VEGF-driven dissociation of the VEGFR2/VE-cadherin complex, reduced the size of myocardial infarct and no-reflow in mice and rabbits, but had no direct effect on cardiomyocytes in vitro in hypoxia, suggesting that Angptl4 may protect the heart by acting on endothelial cells, without changing the vitality of cardiomyocytes [9]. The gene discussed is KDR; the disease is myocardial infarction.