The classic clinical manifestations of TTP include the pentad of MAHA, thrombocytopenia, neuropsychiatric symptoms, fever, and renal failure.[1] The pathogenesis of TTP involves endothelial dysfunction caused by autoantibodies that inhibit the metalloprotease ADAMTS-13, which cleaves von Willebrand factor (VWF). This evidence concerns the gene VWF and endothelial dysfunction.