VEGF stimulation is necessary for induction of bAVM formation in adult mice.25, 26, 27 VEGF neutralization prevented and normalized AVM in an animal model for hereditary hemorrhagic telangiectasia 2 (HHT2), an autosomal‐dominant disorder characterized by telangiectasia and AVMs in multiple organs.28 Bevacizumab (an antihuman VEGF antibody) treatment inhibits the bAVM formation and progression.29 Furthermore, intravenous injection of an adeno‐associated viral vector expressing sFLT1 (the extracellular domain of VEGF receptor 1) attenuated the phenotype severity of bAVMs in mice.30 The gene discussed is VEGFA; the disease is telangiectasis.