TTP results from innate or acquired deficiency of ADAMTS13 (a disintegrin-like and metalloproteinase with thrombospondin type 1 motif 13), a protease that cleaves von Willebrand factor multimers, the deficiency of which results in unusually large von Willebrand factor multimers and a risk of platelet thrombi in small vessels with high shear rates [1]. The gene discussed is ADAMTS13; the disease is thrombotic thrombocytopenic purpura.