Elevated SUA causes endothelial dysfunction by inhibiting NO production and preventing reactive oxygen species formation [41], overproduction of mitochondrial Na(+)/Ca(2+) exchanger-mediated mitochondrial calcium [42], activating renin–angiotensin system [43], causing proinflammation by stimulating monocyte chemoattractant protein-1 [44], vascular smooth muscle cell proliferation [45], platelet aggregation [46], and endothelin increase [47], which eventually contributing to both vascular complications. The gene discussed is CCL2; the disease is endothelial dysfunction.