Among them, GPR-109A can inhibit NF-kB activation and pancreatic β cell inflammation, and the increased expression of GPR-109A in renal injury models can alleviate proteinuria, stabilize glomerular basement membrane podocytes, and alleviate glomerular sclerosis and kidney inflammation (58) (Figure 2). This evidence concerns the gene NFKB1 and glomerulosclerosis.