Studies have shown that in glomerular endothelial cells, high glucose stimulation can induce expression of chemerin, which can promote activation of cytokines through the p38 MAPK signaling pathway (20), and DN patients as well as mice models show increased levels of chemerin expression, and suppressing ChemR23 (receptor for chemerin) alleviates DN damage (21). The gene discussed is CMKLR1; the disease is liver dysplastic nodule.