Our previous study has found that MG132 could depress the activation of NF-κB inflammatory signaling through inhibiting the IκBα sumoylation and ubiquitination, and could inhibit the histone ubiquitination and induce apoptosis in rat glomerular mesangial cells induced by high glucose [13, 20] Renal fibrosis in diabetic nephropathy was induced by activation of the TGF-β signaling pathway, which mediates cell proliferation and differentiation, but whether the proteasome inhibitor could treat diabetic nephropathy by blocking ubiquitin degradation of Smad7 was not reported. This evidence concerns the gene NFKB1 and diabetic kidney disease.