Abstract
In this issue of Blood, Podoplelova et al reveal how structural features of procoagulant platelets, generated in response to strong agonists, eg, thrombin and collagen-related peptides, provide an extensively folded surface area for the membrane-dependent assembly of tenase and prothrombinase complexes and subsequent thrombin generation. In brief, the structural features of a small, specialized region of the surface of procoagulant platelets, termed the “cap,” likely contribute strongly to localized amplification of coagulation in thrombosis.