Histologically, progressive kidney disease is marked by renal fibrosis and glomerulosclerosis.4, 23 It is well known that α‐SMA is the marker of cell transdifferentiation, including epithelial–mesenchymal transition (EMT) and fibroblast activation into myofibroblast, which importantly contributes to the progression of CKD.24, 25 Our results suggest that FGF1 treatment may be involved in the relatively early stage of pathogenic process of DN via ameliorating tubulointerstitial damage. The gene discussed is ACTA1; the disease is glomerulosclerosis.