Along with this concept, one hypothesis for explaining the etiology of HHT is that a deficient BMP9/ALK1/endoglin pathway might lead to re-activation of angiogenesis leading to endothelial hyperproliferation and therefore vasodilation, endothelial cell hypermigration and arteriovenous malformation [84]. The gene discussed is ALK; the disease is hereditary hemorrhagic telangiectasia.