In contrast, occlusive arterial thrombi, that form under high shear rate conditions, can form over collagen exposed after plaque rupture to capture von Willebrand factor (vWF) that, in turn, aggregates platelets to form a white clot.8, 9In the case of arterial thrombosis, a stenotic atherosclerotic plaque is the responsible for creating pathologically high wall shear rates ranging from 5,000 to 100,000 1/s, much higher than the typical wall shear rate of <1,000 1/s found in normal arteries.10, 11When a plaque cap ruptures, prothrombogenic collagen from the extracellular matrix is exposed. The gene discussed is VWF; the disease is Venous thrombosis.