Dear editor, Diabetic kidney disease (DKD) is the leading cause of chronic kidney disease (CKD) and end-stage kidney disease in many countries. Inflammatory targets can prevent the progression of DKD and CKD. Recent studies validate this by demonstrating that the inflammatory-associated transcription factor transforming growth factor beta (TGF-β) and the complement system act synergistically to activate the NLRP3 inflammasome, which influences the progression of CKD [1]. Interleukin receptor antagonists as a novel therapy, including Tozorakimab, providing opportunities for further drug development. Hofherr et al. [2] findings that interleukin (IL)-33 pathway may reduce inflammation in the glomerular endothelium of patients with DKD and highlight the potential clinical benefit of IL-33 blockade by tozorakimab in patients with DKD. These findings provide a solid foundation for the broader application of interleukin receptor antagonists.