The possible underlying mechanism might be explained by the excessive prooxidant effect in a hyperuricemia environment that leads to endothelial dysfunction, increased activity of xanthine oxidase, increased oxidative stress, inappropriate activation of the renin–angiotensin–aldosterone system, impaired renal autoregulatory response, and release of proinflammatory chemokines (38). The gene discussed is XDH; the disease is hyperuricemia.