The roles of CCM genes in non-endothelial cells (e.g. neuroglia, pericytes, smooth muscle cells, astrocytes) are much less studied and their contributions to CCM disease are unclear, as while loss of neural CCM3 does produce dilated vasculature and vascular lesions in mice [49], neural or smooth muscle-specific deletion of CCM2 does not recapitulate CCMs [48,50]. The gene discussed is CCM2; the disease is cerebral cavernous malformation.