We first considered the role of the highest expressed platelet integrin αIIbβ3, using blood from patients with Glanzmann thrombasthenia lacking this integrin.25 Subsequently, we examined the effect of flow disturbance and studied the contribution to leukocyte responses of platelet activation markers (CD62P and CD40L) and platelet-released chemokines. This evidence concerns the gene SELP and Glanzmann thrombasthenia.