 Heme oxygenase-1 HO-1 is a factor associated with higher risk of developing some vascular disease and also a rate-limiting enzyme in heme degradation, leading to the generation of free iron, biliverdin, and carbon monoxide CO. CO exerts potent antiproliferative and anti-inflammatory effects in the vascular walls, thereby influencing neointimal formation after vascular injury. In addition, biliverdin is subsequently metabolized to bilirubin by the enzyme biliverdin reductase. Therefore, induction of HO-1 elicits potent anti-inflammatory, antiproliferative, antithrombotic, and antioxidant effects in the circulation via the generation of CO and bilirubin. Interestingly, recent study found that a long guanidine thymidine dinucleotide repeat GT n 30 in the HO-1 promotor, which is linked to impaired inducibility, is associated with a higher frequency of vascular access failure. 