Defects in vascular ALK1 signaling are implicated in its pathogenesis, and heterozygous variations of the genes encoding endoglin (ENG), activin A receptor like type 1 (ACVRL1), SMAD family member 4 (SMAD4) and bone morphogenetic protein 9 (GDF2) have been identified to be causative in HHT [2]. The gene discussed is ALK; the disease is hereditary hemorrhagic telangiectasia.