The formula inhibited the expression of smurf2 and Smad3 in the kidney tissue of DKD rats, upregulated the expression of Smad7, improved the degradation of IκBα and the nuclear translocation of NF-κB (p65), reduced the protein and mRNA levels of TGF-β1, IL-1β, IL-6, and MCP-1, and effectively protected against renal fibrosis and inflammatory damage in DKD.[67] Therefore, inhibiting smurf2-mediated Smad7 ubiquitin degradation may be the central mechanism by which Tangshenfang inhibits TGF-β1/smad3-mediated renal fibrosis and NF-κB-dependent renal inflammatory injury in DKD. Here, NFKB1 is linked to diabetic kidney disease.