The accumulation of ROS and RNS in the DN microenvironment leads to the impairment of the mitochondrial electron respiratory chain, as well as the disruption of the NAD+/NADH balance, which downregulates SIRT3 expression and activity, affects the reprogramming of mitochondrial energy metabolism, and drives the sustained activation of the pro-inflammatory macrophage phenotype type M1, which mediates the persistent generation of chronic inflammation [13], thus exacerbating the progression of DN. The gene discussed is SIRT3; the disease is liver dysplastic nodule.