On this regard, it should be noted that the molecular mechanisms responsible for CCM lesions development (namely increased RhoA activity56, augmented MEKK3/KLF2,4 signalling43, and abnormal activation of the TGFβ/BMP/SMAD pathway44) may be influenced by additional mechanisms such as the behaviour of pericytes. The gene discussed is RHOA; the disease is cerebral cavernous malformation.