Defects or deficiencies (<10%) of ADAMTS13 leads to the accumulation of UL‐vWF multimers in the circulation, eventually forming vWF‐platelet‐rich thrombi under high shear stress conditions manifesting phenotypically as TTP [2, 3, 4, 5]. Here, ADAMTS13 is linked to thrombotic thrombocytopenic purpura.