Furthermore, Cai et al. reported that animals possessing the double mutation of hph1 and NOX1, NOX2, p47phox, or NOX4 had reduced AAA incidence and abdominal aortic expansion after Ang II infusion due to reduced superoxide production, as well as improved NO and H4B bioavailability, and restored eNOS coupling activity compared to hph1 mice. This evidence concerns the gene NOS3 and triple-A syndrome.