We and others have demonstrated that an inflammatory component plays a role in triggering DVT.13,14 Local hypoxia may result in release of Weibel–Palade body (WPB) constituents, such as von Willebrand factor (vWF) and P-selectin, to the endothelial surface leading to recruitment of platelets and leukocytes.15 Platelets can contribute to thrombosis initiation likely by providing their procoagulant surface to clotting factors, whereas neutrophils support DVT propagation by producing neutrophil extracellular traps.16,17. Here, SELP is linked to deep vein thrombosis.