Indeed, we observed dysregulation of KRIT1, related to cerebral cavernous malformations (CCM) [49], APLN, related to lymphatic malformations [50], GNA11 [51] related to capillary malformations and BMPR2, related to arteriovenous malformations and hereditary pulmonary arterial hypertension (HHT) [52]. This evidence concerns the gene GNA11 and hereditary hemorrhagic telangiectasia.