Approximately 85% of HHT cases are linked to heterozygous loss-of-function mutations in the transforming growth factor beta  (TGFβ)  cell surface receptors activin receptor-like kinase 1 (ALK1, HHT2) or endoglin (ENG, HHT1) [9, 10]. This evidence concerns the gene TGFB1 and hereditary hemorrhagic telangiectasia.