Several studies have reported that uric acid induced renal tubule epithelial cells and endothelial dysfunction and interstitial fibrosis [46], and activated inflammation in the kidney through oxidative stress, epithelial-to-mesenchymal transition, regulating NLRP3 inflammasome-mediated IL-1β secretion [47], reducing levels of SUMO-PPARγ, etc. [48]. The gene discussed is IL1B; the disease is endothelial dysfunction.