Etiologies include autoantibodies that directly inhibit the activity of VWF or increase clearance from circulation [3], shear-stress proteolysis (e.g., aortic stenosis, cardiac devices) [4], and adsorption of VWF onto cells that express the VWF receptor glycoprotein Ib (e.g., Wilm’s tumors) [5]. Here, VWF is linked to aortic stenosis.