These findings are important because both PNA formation and platelet activation are increased in ischemic stroke and are involved at several levels in the pathogenesis and severity of stroke.51 Although PNAs have been widely used as a surrogate marker for systemic inflammatory responses,52 the pathophysiological importance of these aggregates is unclear.53 The fact that AnxA1 reduced endothelial PNA formation in the brain further supports the concept of this protein acting as a key resolving mediator of thromboinflammation after cerebral I/RI. This evidence concerns the gene ANXA1 and stroke disorder.