Enhanced NF-κB acetylation level was present in both diabetic rats and HG-treated RMC leading to DN in another study, which can be dampened by 3,5-diiodothyronine (T2) involved regulation of SIRT1 [46]; acetylation of NF-κB p65 and STAT3 was increased in both mice and human diabetic kidneys and AGEs induced human podocytes, suggesting their critical roles in DN [47]. Here, SIRT1 is linked to liver dysplastic nodule.