Additionally, Bravi and co-workers reported that TGF-β1 signaling is triggered downstream following β-catenin activation in CCM3-deficient endothelial cells both in vitro and in vivo and leads to endothelial-to-mesenchymal transition, implying TGF-β/BMP signaling as crucial regulators for CCMs disease progression69. This evidence concerns the gene PDCD10 and cerebrocostomandibular syndrome.