The pathophysiological mechanisms underlying TTP mainly include the formation of ultra-large von Willebrand factor (vWF) in circulation, leading to spontaneous platelet aggregation (Moake, 2002; Lämmle and George, 2004; Sadler et al., 2004; Kremer Hovinga et al., 2017). The gene discussed is VWF; the disease is thrombotic thrombocytopenic purpura.