Since endothelial cells are crucial for coagulation regulation through anticoagulant factor production, including thrombin inhibitors and elements of the protein C pathway such as thrombomodulin and endothelial protein C receptor (EPCR) (18, 19), this persistent endothelial inflammation and damage may disrupt this regulation, contributing to coagulopathy in LC. This evidence concerns the gene PROCR and laryngotracheoesophageal cleft.