Inhibition of the GPIb-vWF axis exerts thrombolytic effects and prevents stroke progression in the absence of intracranial bleeding. Ischemic stroke is mainly caused by thromboembolic occlusion of a major cerebral artery (top panel, left). Treatment with tPA leads to recanalization of the occluded macrovessel, but in the study by Momi et al,¹  it did not prevent thrombo-inflammation in the microcirculation and further stroke progression. Inhibition of platelet GPIIb/IIIa (top panel, anti-GPIIb/IIIa) has no thrombolytic effect but causes intracranial hemorrhage, which is even worse when given in combination with tPA (tPA + anti-GPIIb/IIIa). In sharp contrast, inhibition of the GPIb-vWF axis induces thrombolysis at early time points after thrombus formation and prevents thrombo-inflammatory damage of the microcirculation and infarct progression (top panel, right). The latter effect is even seen at later time points when the thrombolytic effect is lost due to thrombus stabilization (not shown).