In angiogenesis, HHT mutations (endoglin and ALK-1) appear to impair recruitment of mural cells to the angiogenic sprout [7,28] at least in part via reduced EC secretion of TGF-β1 [29,30] and/or reduced TGF-β1 induced responses [7,29] resulting in defective mural cell stabilisation of the nascent vessel and persistent, excessive, EC proliferation. The gene discussed is ENG; the disease is hereditary hemorrhagic telangiectasia.