The proposed mechanisms include: EnD with a disruption in nitric oxide production, elevated levels of homocysteine with an inflammatory mediator, and systemic inflammation with an increase in high sensitivity C-reactive protein and lipoprotein A. Lipid metabolism dysregulation with adiponectin, gut microbiota with endotoxins, and bile acids and environmental factors like insulin resistance and/or various genetic factors have also been described to contribute to the common pathophysiology between NAFLD and CAD. This evidence concerns the gene ADIPOQ and metabolic dysfunction-associated steatotic liver disease.