Studies have shown that p-Smad2 and p-Smad3 expression levels increase significantly in patients with chronic kidney disease and animal models of renal fibrosis, thereby activating the TGF-β1/Smads signaling pathway and simultaneously increasing the expression of α-SMA protein, a marker of mesenchymal cells, the expression level of which reflects the degree of renal fibrosis [36–38]. This evidence concerns the gene SMAD2 and chronic kidney disease.