Our hypothesis was derived from the subsequent results of previous clinical and experimental studies: (1) uric acid stimulated renal inherent cells, such as mesangial cell, tubular cell, and endothelial cells, to produce inflammatory cytokines (20–23); (2) xanthine oxidase inhibitor treatment decreased uric acid level, resulting in attenuating macrophage infiltration to the kidney in diabetic rat (24); and (3) there was positive correlation between serum uric acid and circulating TNFR levels in patients with IgA nephropathy and diabetes (16, 17). The gene discussed is TNFRSF1A; the disease is diabetes mellitus.