CDH17 and cerebral cavernous malformation: In particular, it is intriguing that the activation of redox signaling complexes at integrin-mediated cell-matrix adhesion sites and cadherin-mediated cell-cell junctions induces opposite effects, leading to assembly of integrin-mediated focal adhesions and disassembly of cadherin-mediated AJs, respectively, followed by morphological transition toward a mesenchymal phenotype (Goitre et al., 2012), which recapitulate almost all the major molecular mechanisms of CCM pathogenesis.