ADAMTS13 cleaves ultra-large, highly reactive VWF multimers into smaller, less active ones, preventing spontaneous platelet-thrombus formation and reducing inflammation.[3] Preclinical animal studies have shown that absence of VWF is protective in ischemic stroke whereas absence of ADAMTS13 worsens disease outcome.[4–6] Increasing clinical evidence also demonstrates a clear association between high VWF-levels and acute ischaemic stroke in patients. The gene discussed is VWF; the disease is ischemic stroke.