It is worth noting that AVMs develop due to a combination of gene mutations in TGF-β signaling with angiogenic induction (via VEGF stimulation or wounding) (Park et al., 2009; Garrido-Martin et al., 2014), supporting the “Two hit mechanism” in HHT. The gene discussed is TGFB1; the disease is hereditary hemorrhagic telangiectasia.