The most common forms of HHT, HHT1 and HHT2, have been linked to mutations in the endoglin (ENG) and activin receptor-like kinase 1 (ACVLR1 or ALK1) genes respectively, both encoding putative receptors for the transforming growth factor-beta (TGF-β) superfamily that play a critical role for the proper development of the blood vessels [4]–[6]. This evidence concerns the gene TGFB1 and hereditary hemorrhagic telangiectasia.