Furthermore, NLRP3 inflammasome was significantly activated, leading to the release of large amounts of IL-1β and IL-18 in eDN, further initiating the inflammatory response in the diabetic kidney.<h4>Conclusions</h4>Our findings identify critical hub genes associated with DN progression and NLRP3 inflammasome activity, providing a theoretical basis and candidate targets for subsequent research. This evidence concerns the gene IL1B and liver dysplastic nodule.