By cleaving the highly reactive ultra-large VWF multimers into smaller, less hemostatically active VWF molecules, ADAMTS13 has been shown to reduce both microvascular thrombosis and inflammation and improve microvascular endothelial dysfunction in experimental models of diabetic nephropathy [11], acute kidney injury [12], myocardial infarction [13], sickle cell disease [14], rheumatoid arthritis [15], stroke [16], and subarachnoid hemorrhage [17]. The gene discussed is ADAMTS13; the disease is endothelial dysfunction.