NOX-driven uncoupling of eNOS mediates hypertension, and,in particular,it is a causal factor for the development of abdominal aortic aneurysm(AAA): genetic knockout of NOX1, NOX2, p47phox, or NOX4prevented formation of AAA, reducing abdominal aortic expansion andrestoring eNOS coupling activity.87 Moreover,ROS avidly react with and inactivate NO and, in the process, producehighly reactive and cytotoxic products.88 Here, NCF1 is linked to triple-A syndrome.