In the laser injury thrombosis model, neutrophils have been reported to interact with the activated endothelium and augment thrombus formation.2 In this model, blocking endothelial intercellular adhesion molecule 1 (ICAM‐1) prevents neutrophil recruitment and consequently greatly reduces both platelet and fibrin accumulation after the vascular injury.2 We therefore examined neutrophil accumulation in Bambi−/− mice using the laser‐induced thrombosis model. Here, ICAM1 is linked to deep vein thrombosis.