This model implies that activation of the quiescent endothelium, for example by inflammation and/or angiogenesis i.e., wounding or VEGF stimulus, will induce excessive vessel sprouting and the development of a broad spectrum of vascular abnormalities such as AVMs the pathological hallmark of HHT (Figure 2; Park et al., 2009; Lebrin et al., 2010; Mahmoud et al., 2010; Chen et al., 2013; Choi et al., 2013). The gene discussed is VEGFA; the disease is hereditary hemorrhagic telangiectasia.