This result echoes the observation that vascular symptoms of HHT patients are due to ENG haplo-insufficiency [43], [44] and that loss of one copy of Eng in a genetically engineered mouse model is sufficient to lead to angiogenesis inhibition in a tumor model [45] and to vascular defects reminiscent of HHT [46]. Here, ENG is linked to hereditary hemorrhagic telangiectasia.