In the pathogenesis of venous thrombosis, stasis is essentially a permissive factor, allowing the normal defense mechanisms of the body to be circumvented. Although a platelet monolayer is an insufficient stimulus for fibrin formation, even in the presence of stasis, trace amounts of an activated clotting factor are highly thrombogenic in an area of retarded blood flow. The available clinical and experimental data suggest that, if thrombin generation is reduced, the great majority of venous thrombi are prevented.