These results contradict our initial hypothesis that the increased AM expression found in HHT patients [10] may be due directly to the mutations of these patients in the ENG or ACVRL1 genes, but seem to suggest a very complex interplay between the AM system and the TGF-β family of peptides and receptors, which includes BMP-9 [26]. Here, ACVRL1 is linked to hereditary hemorrhagic telangiectasia.