Genetic polymorphisms have also been linked to thrombosis in APS patients, including variants of coagulation factors, anti-thrombotic and fibrinolytic molecules [i.e., FXIII, tissue factor pathway inhibitor (TFPI), type-I plasminogen activator inhibitor (PAI-1)] inflammatory mediators [i.e., tumor necrosis factor alpha (TNFα)], parameters related to platelet activity (i.e., platelet FC receptor IIa, platelet glycoproteins GP Ia/IIa and GP IIb/IIIa), endothelial factors (i.e., thrombomodulin), etc. (9). Here, TNF is linked to autoimmune polyendocrinopathy.