Among the various forms of TMA, thrombotic thrombocytopenic purpura (TTP) is attributed to a severe deficiency of a disintegrin and metalloprotease with thrombospondin type I repeats 13 (ADAMTS13) activity, leading to the accumulation of high-molecular-weight von Willebrand Factor multimers in plasma, resulting in excess platelet aggregation in multiple organs [1]. This evidence concerns the gene ADAMTS13 and thrombotic thrombocytopenic purpura.