To gain insight into the mechanism underlying how specific FOXO3A deletion mediates arterial endothelial dysfunction, we generated FOXO3A-knockout (KO) human ECs by specifically knocking out FOXO3A in human embryonic stem cells (hESCs) using the TALEN-facilitated homologous recombination technique (Fig. 4a and Supplementary Fig. 11a). This evidence concerns the gene FOXO3 and endothelial dysfunction.