ADAMTS13 and thrombotic thrombocytopenic purpura: TTP is distinguishable from other TMAs due to different pathophysiology and treatment options, and mainly due to patients’ severe deficiency of ADAMTS13, a metalloproteinase, disintegrin, with a thrombospondin type 1 motif, member 13, which processes the von Willebrand factor (VWF) multimers to prevent them from interacting with platelets and form microvascular thrombi [2,3].