RHOA and cerebral cavernous malformation: Finally, while the primacy of inflammatory signaling to CCM formation has yet to be formally established, it is important to note that the wide variety of molecular mechanisms attributed to CCM formation, including down-regulation of cell-cell contacts, altered cell-matrix adhesion, activation of RhoA signaling and cytoskeleton contractility, endothelial to mesenchymal transition, altered expression levels and activity of various transcription factors, increased oxidative stress, and angiogenesis, all fit comfortably under the umbrella of known inflammatory signaling mechanisms.