“…To explain this paradox, the need for a trigger such as inflammation, vascular injury, angiogenic stimuli, or ischemia has been postulated ( Park et al, 2009 ; López-Novoa and Bernabeu, 2010 ; Choi et al, 2014 ). In HHT1, this trigger would synergize with endoglin haploinsufficiency to generate the vascular lesion ( Lopez-Novoa, 2012 ; Choi et al, 2014 ). Interestingly, those stimuli are usually associated with the upregulated expression of endoglin in endothelial cells and an inflammatory cell infiltrate ( Torsney et al, 2002 ; López-Novoa and Bernabeu, 2010 ), suggesting the need of both, endoglin function and leukocyte infiltration, in the vascular repair/remodeling process.…”