Furthermore, TTP is typically characterised by vWF in non-inflammatory, platelet-rich “white” thrombi [7], unlike the inflammatory, fibrin-rich “red” thrombi with C5b-9 deposition, caused by aberrant alternative pathway mechanisms of complement activation more commonly seen in HUS and TA-TMA [3, 7, 10, 11]. The gene discussed is VWF; the disease is thrombotic thrombocytopenic purpura.