In patients with asthma, hyper-coagulation is activated through mechanisms of (1) increased expression of the tissue factor (TF), (2) decreased activity of anticoagulant protein C (PC) system, and (3) inhibition of fibrinolysis through over-production of plasminogen activator inhibitor type 1 (PAI-1) [4,9,10,11]. The gene discussed is F3; the disease is asthma.