To investigate the mechanism responsible for AS-associated hypercoagulability, the enzymatic activities of several coagulation factors, including FVIIa, FXIa, FXIIa, kallikrein, and thrombin, were compared between plasma from healthy volunteers and atherosclerotic patients who have coronary heart disease (CHD) and display angiographically visible luminal narrowing (Supplementary information, Table S1). The gene discussed is KLK4; the disease is thrombophilia.