In the progression of DKD, GSDMD-N acts as a perforating protein, forming pores in proper renal cells, gradually triggering cell death, releasing pro-inflammatory factors, such as IL-1β and IL-18, and aggravating RF, including GS and renal tubulointerstitial fibrosis (Gu et al., 2019). This evidence concerns the gene IL1B and diabetic kidney disease.