The functional remit of XOR has extended well beyond ROS and UA synthesis over the past 10–15 years, with the growing appreciation that in many pathological settings, particularly for metabolic disease and CVD, when the eNOS-dependent pathway is dysfunctional, XOR acts as a critical NO2−-reductase [9], [[64], [65], [66]]. The gene discussed is XDH; the disease is Other metabolic disease.