Remarkably, whereas there is evidence that reduced endothelial cell–pericyte association and basement membrane alteration are integral parts of both CADASIL [68,69] and CCM [70,71] pathogenesis, the co-occurrence of CADASIL and CCM lesions has been also reported, suggesting a common pathogenetic mechanism driven by NOTCH3 mutations leading to microangiopathy [72]. Here, NOTCH3 is linked to cerebral cavernous malformation.