In reports of diabetic nephropathy, the acetylation levels of p65 NF-κB and STAT3 are elevated [17], and SIRT1 can confer reno-protective effects by inhibiting renal inflammation, apoptosis, oxidative stress, and fibrosis through deacetylation of STAT3 and p65 NF-κB target proteins to stop the progression of diabetic kidney disease to end-stage renal disease [18, 19]. The gene discussed is STAT3; the disease is diabetic kidney disease.