Our previous study reported that the imbalance of the ADAMTS13 enzyme–VWF substrate worsened according to LC progression [2,8,9,12], and that patients with LC with hepatic encephalopathy, ascites, and hepatorenal syndrome (HRS) had a more significant imbalance in the ADAMTS13 enzyme–VWF substrate than those without these manifestations [2,8,9]. Here, VWF is linked to laryngotracheoesophageal cleft.