The pathophysiology of TTP is driven by a disintegrin and metalloprotease with thrombospondin type I repeats-13 (ADAMTS13) deficiency (activity levels ≤ 10%) leading to formation of platelet thrombi, resulting in thrombocytopenia,2,3 to hemolytic anemia with fragmented red blood cells (schistocytes), microvessel occlusion, and tissue injury.4 This evidence concerns the gene ADAMTS13 and thrombotic thrombocytopenic purpura.