Our previous studies also demonstrated that Toll-like receptors, predominantly TLR2 and TLR4, recognize endogenous DAMPS, such as AGEs, HSP60, HSP70, and MCP-1 induce inflammatory responses via the nuclear factor-κB (NF-κB) signaling pathway in DKD; Moreover, we also proved that one member of NLRs: NLRP3 could mediated inflammation in podocytes under high glucose and DKD mice, resulting in the injury of podocytes and kidney, which is consistent with our previous study on the TLR signaling pathway. The gene discussed is NFKB1; the disease is diabetic kidney disease.