A study of 164 patients with NS reported elevated levels of vWF, syndecan-1, and e-selectin, with significantly higher vWF levels in those who developed VTE.9 Similarly, elevated thrombomodulin and E-selectin in patients with NS, further supporting the presence of endothelial activation and injury in this population.8 Endothelial integrity plays a crucial role in maintaining vascular homeostasis, and its disruption fosters a prothrombotic state by impairing anticoagulant mechanisms and promoting coagulation activation.43 In NS, endothelial dysfunction may further amplify hypercoagulability. The gene discussed is VWF; the disease is endothelial dysfunction.