A switch of this balance to the benefit of augmented responses toward TGFβ is a hallmark of endothelial cell (EC) dysfunction and precondition to several vascular diseases, including cerebral cavernous malformation (CCM) [2], hereditary hemorrhagic telangiectasia (HHT) [3], and pulmonary arterial hypertension (PAH). Here, TGFB1 is linked to cerebral cavernous malformation.