A gain-of-function mutation in the A1 domain causes spontaneous binding of vWF to GP1bα receptors on platelets, causing increased clearance of vWF multimers and platelets, and, additionally, abnormal vWF can modify megakaryocytopoiesis, both of which result in thrombocytopenia [1,2]. Here, VWF is linked to Thrombocytopenia.