In the pathogenesis of NAFLD/NASH, the role of NO is debatable: while the NO-AMP-activated protein kinase (AMPK)-peroxisome proliferator-activated receptor α (PPARα) signaling pathway is crucial for the control of hepatic fatty acid oxidation [12], the excess production of NO content, which leads to nitrosative stress, is correlated with the severity of NAFLD [13]. This evidence concerns the gene PPARA and metabolic dysfunction-associated steatotic liver disease.