Vessel wall injury and subsequent blood extravasation activates a series of local biological processes to prevent excess blood loss via the formation of hemostatic plug strictly restricted at the site of vascular injury with minimal or no extension in the vessel lumen. 1 In the vast majority of cases, a catastrophic systemic activation of these processes is contained by specific mechanisms. As opposed to hemostasis, thrombosis is characterized by the deregulated clot formation, various degrees of vessel occlusion, tissue ischemia, and necrosis. 1 A large body of accumulating experimental and clinical data over the past 20years has clearly indicated the reciprocal relationship and dynamic interplay between inflammation and thrombosis. 2–5 Today, targeting inflammation to prevent thrombotic events represents a realistic and promising therapeutic approach. 6 Among immune cell subsets that are implicated in multiple molecular pathways during inflammatory response, neutrophils have a crucial role, recruited first to the site of injury following instructive signals from the tissue environment. 7

The very first observation linking neutrophils with thromboinflammation was reported almost 70years ago describing granulocytes as a main component of clotted blood in patients suffering from active lupus erythematosus. 8 During the following years, although several studies had described the accumulation of neutrophils at the site of thrombus formation, these cells remained neglected and less studied in many throm-