Accordingly, release of EVs by endothelial cells is thought to reflect endothelial activation and/or stress [43, 86], and has been reported elevated in MS [87]—the EVs in question being designated EMPs and identified as two subtypes by their respective expression of CD31 (PECAM-1) and CD51 (vitronectin receptor). The gene discussed is PECAM1; the disease is myeloid sarcoma.