Interactions between platelets and leukocytes link critical thrombotic and inflammatory events that control an array of cardiovascular syndromes. In atherosclerosis alone, inducible gene expression in platelets and leukocytes modulates the initiation and development of vulnerable plaques that increase a patient's risk for acute coronary events. Interruption of gene expression pathways that are triggered when platelets adhere to leukocytes may be a new target for therapeutic intervention. Recent evidence indicates that dipyridamole, an old drug with a diverse history, differentially inhibits gene expression in platelet-leukocyte aggregates by exerting its effect at distinct molecular checkpoints.