Moreover, KLF2 overexpression via an adenoviral vector reverses patient-serum-induced endothelial dysfunction and controls the expression of genes related to endothelial dysfunction with the upregulation of vascular homeostasis related genes (KLF2, NOS3, and THBD) and antioxidant genes (GCLM and NQO1) and reduction of the expression of pro-inflammatory (VCAM1, CCL2, and DKK1), vasoconstrictive (EDN1), and pro-angiogenic (ANGPT2) genes. This evidence concerns the gene NOS3 and endothelial dysfunction.