Interestingly, accumulating evidence suggests that patients with advanced forms of NAFLD have an increased production of pro-thrombotic factors by the liver, like plasminogen activator inhibitor-1 (PAI-1) or factor VIII and reduced levels of anticoagulant factors [3], consequent to the chronic inflammation with oxidative injury, necrosis, and apoptosis [4–6]. This evidence concerns the gene SERPINE1 and metabolic dysfunction-associated steatotic liver disease.