The mechanisms that contribute include sympathetic activation resulted from hypoxemia15,27 which in turn leads to platelet activation and the release of angiotensin II, pulmonary vasoconstriction due to the release of thromboxane A2 from platelets,6,28,29 hypercoagulability secondary to an increase in the plasma levels of platelet factor-4 and β-thromboglobulin29 and increase in platelet-fibrinogen binding resulted from the overexpression of adhesion molecules such as P-selectin, glycoprotein Ib and glycoprotein IIb/IIIa in platelets.5,30. The gene discussed is SELP; the disease is thrombophilia.