The pathogenesis of HHT is heterozygous mutation in one of two genes, endoglin (ENG) or activin receptor-like kinase type 1 (ALK-1), which are both associated with the transforming growth factor β (TGF-β) superfamily signaling pathway expressed mostly in the vascular endothelium [8, 9]. This evidence concerns the gene ENG and hereditary hemorrhagic telangiectasia.