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Nonalcoholic fatty liver disease (NAFLD) israpidly becoming the most common cause of fatal liverdiseases such as cirrhosis, liver cancer, and indications fororthotopic liver transplantation. Given its high prevalence,the absence of FDA-approved drugs for NAFLD isnoticeable. In the pathogenesis of NAFLD, it is well knownthat mitochondrial dysfunction arises as a result of changesin ETC complexes and the membrane potential (Dwm), aswell as decreased ATP synthesis. Due to their fundamentalrole in energy metabolism and cell death decision, alterationsin mitochondria are considered to be critical factorscausing NAFLD. Reduced levels of b-oxidation, alongwith increased lipogenesis, result in lipid accumulation inhepatocytes, and the subsequent production of reactiveoxygen species and hepatocyte injury, which contribute tohepatic inflammation and fibrosis through the activations ofKupffer cells and hepatic stellate cells. Here, we review thelatest findings describing the involvement of mitochondrialprocesses in the development of NAFLD and discuss thepotential targets against which therapeutics for this diseasecan be developed.