Determining whether inhibition of Golgi reorientation downstream of RHO is involved in initiating the formation of vascular lesions in cerebral cavernous malformations, as well as revealing the mechanism through which Golgi-localised MSTs regulate reorientation, could prove to be crucial for devising novel therapeutic approaches against the early molecular events that trigger the disease. The gene discussed is RHO; the disease is famililal cerebral cavernous malformations.