Contact of the blood with a foreign surface such as glass initiates clotting not only by disruption of platelets but by the activation of plasma clotting factors. Many explanations have been advanced for the increased coagulability of the plasma. Contact with glass has been said to remove a lipid antithromboplastin (anti-cephalin) (1-3), to remove a protein inhibitor of prothrombin (4-6), to activate a plasma thromboplastin precursor (7-10), more specifically, the antihemophilic B factor (Christmas factor') (11), and to convert an in-