Glycoprotein VI (GPVI), the main platelet receptor for collagen, has emerged as a new target for antithrombotic therapy because its genetic deficiency or pharmacological blocking inhibits platelet aggregation and experimental thrombosis without increasing bleeding time. While these data have stimulated the development of new antiplatelet drugs targeting GPVI, recent findings have indicated that GPVI is essential for repair of neutrophilinduced vascular injury in various inflamed organs and tissues. It thus appears important to assess and anticipate the yet uninvestigated risk of inflammation-induced bleeding under GPVI antagonists, especially considering that inflammation is a component of various thrombotic diseases. In that respect, it is worth noting that neutrophil mobilization is a predictor of hemorrhagic transformation of ischemic stroke and contributes to intraplaque hemorrhage, which is known to precipitate plaque rupture and the clinical expression of atherosclerosis.