HMGB1 and intracranial embolism: The strong colocalization of HMGB1 and NETs in cerebral thromboemboli, together with the recent finding of a local increase in HMGB1 plasma levels related to the extent of neutrophil recruitment in the ischemic cerebral circulation of stroke patients [5], supports the notion that extracellular HMGB1 derived from activated platelets and NETosed neutrophils is an early mediator in thrombus growth and cerebral embolism.