Therefore, to summarize, thyroid hormones act at different levels in determining hypercoagulability: they cause an increase in FVIII, in particular in its B subunit (FVIIIB), FIX, vWF, fibrinogen and PAI-1, acting directly on hepatocytes and endothelial cells, causing a state of hypercoagulability and hypofibrinolysis [11,85,89,90,91]. This evidence concerns the gene VWF and thrombophilia.