ENG and vascular malformation: Our findings support the idea that an almost complete loss of endoglin is a prerequisite for the development of vascular lesions as previously suggested [26,45], but also implies that a local transient release of the receptor from the cell surface during inflammation or a second local mutation in the wild-type allele might not be necessary for the development of vascular malformations, at least in tissues such as the skin [26,33].