Our results identified pathways related to angiogenesis (VEGF and NOTCH signaling), and endothelial cell–cell contact (platelet and endothelial cell adhesion molecule 1 [PECAM1], cadherin 5 [CDH5], and junctional adhesion molecule [JAM]) showed large functional difference between CCM and non-lesional control tissue (p < 0.05, FDR corrected) (Fig. 5a). The gene discussed is CDH5; the disease is cerebral cavernous malformation.