More importantly, we demonstrated that the podocyte-specific knockout of Sirt1 in db/db mice led to higher levels of p65 and STAT3 acetylation and resulted in greater degree of proteinuria and kidney injury than in control db/db mice, implicating SIRT1 as a key inhibitor of the NF-κB- and STAT3-induced inflammatory responses in DKD (33). The gene discussed is NFKB1; the disease is diabetic kidney disease.