Although measurement error in insulin resistance cannot be excluded, as we previously summarized [13], several mechanisms may be involved in the sUA-CVD association, including elevated sUA (1) being a marker of xanthine oxidoreductase activity and oxidative stress related to atherosclerosis; (2) mediating proinflammatory pathways; (3) inducing endothelial dysfunction; (4) activating the renin–angiotensin system; (5) resulting from renal dysfunction leading to reduced sUA clearance (also suggested by Knowles and Reaven [41]). This evidence concerns the gene REN and endothelial dysfunction.