KNG1 and ischemic stroke: Given the multiple roles for bradykinin in the neurovascular unit described so far including increase in BBB permeability, inflammatory cytokines upregulation, release of glutamate by astrocytes and microglial activation (all potential pathogenic players in ischemic stroke) (17), it is tempting to speculate that the generation of bradykinin triggered by tPA administration participates in its deleterious effects.