This is consistent with our results showing that the abnormal phenotype in eng mutants can be abrogated by inhibiting Vegf signalling, in agreement with other studies in mouse models of HHT (Han et al., 2014; Jin et al., 2017; Tual-Chalot et al., 2020) and current clinical therapies targeting VEGF in HHT patients (Dupuis-Girod et al., 2012). This evidence concerns the gene VEGFA and hereditary hemorrhagic telangiectasia.