Both types account for the majority of the genetically diagnosed HHT population (85% approximately), although recent reports point to mutations in other components of the TGF-β signaling pathway, such as SMAD4 (MIM #175050) and BMP9 (GDF2) (MIM #615506), in a reduced HHT population [1]. Here, SMAD4 is linked to hereditary hemorrhagic telangiectasia.