Two studies have suggested a mechanistic role of elevated vWF levels in MPN-related thrombosis: JAK2V617F-positive endothelial cells from both human and mouse models led to a prothrombotic state via increased surface expression of the adhesion molecule P-selectin and vWF, as well as increased release of vWF [26, 27]. Here, SELP is linked to myeloproliferative neoplasm.