Supporting the role of EC activation or dysfunction in GVHD pathogenesis, histologic analysis of patients with cutaneous GVHD showed evidence of increased adhesion markers VCAM-1, endothelial leukocyte adhesion molecule-1 (ELAM-1) and vWF extravasation (82), while upregulation of vWF and thrombomodulin (TM) levels was observed in patients who developed acute GVHD post-transplant compared to those who did not (83), and serum levels of sICAM-1 and skin biopsies of E-selectin were both increased in acute GVHD patients (84). The gene discussed is THBD; the disease is acute graft versus host disease.