Consistent with this possibility, there is also evidence that CCM proteins control DLL4-NOTCH3 signaling between the endothelium and pericytes, which is important to maintain a quiescent vascular phenotype and prevent angiogenesis [73], suggesting that NOTCH3 mutations causing deregulated DLL4-NOTCH3 signaling may indeed contribute to the pathogenesis of both CADASIL and CCM disease. This evidence concerns the gene DLL4 and cerebral cavernous malformation.