In NAFLD, adaptive responses of mitochondria to lipid overload result in compensatory enhancement in the oxidative capacity and a decrease in the energy coupling efficiency, leading to lipid deposition and insulin resistance.[201, 205] Typical features of mitochondrial dysfunction in NAFLD include, ROS bursts, depletion of antioxidant defense systems (such as SOD2 and GPX), mitochondrial DNA damage, and increased proton leakage.[239, 240, 241, 242]. The gene discussed is SOD2; the disease is metabolic dysfunction-associated steatotic liver disease.