Adipose tissue may impair fibrinolysis through direct production of coagulation factors (such as PAI-1 and thrombin activatable fibrinolysis inhibition), dysmetabolism-associated nonalcohol liver steatosis may alter the hepatic synthesis of haemostatic factors, and adipokines may affect platelet function; insulin resistance-associated low-grade inflammation and endothelial dysfunction may modulate the genetic expression, activity, and interactions of haemostatic factors [27, 31–33]. The gene discussed is SERPINE1; the disease is endothelial dysfunction.