Increased ROS production has been demonstrated in vitro and in vivo in a variety of mouse models of DN [12], and ROS leads to marked dysfunction of mitochondrial respiratory chain complex I (NADH-ubiquinone oxidoreductase), as well as a decrease in the activity of complexes II, IV, and V (ATP synthases), accompanied by a decrease in the NAD+/NADH ratio [96,97], as the NAD-dependent deacetylase Sirtuin3 (SIRT3) plays a key role in deacetylating and modifying the enzymatic activity of respiratory chain complexes I, II, and III (ubiquinol–cytochrome c oxidoreductase). The gene discussed is SIRT3; the disease is liver dysplastic nodule.