In this study, we provided critical insights into our previous findings, including comprehensive characterization of vascular lesions in the brain of NgbrECKO mice at both postnatal and adult stages, demonstrating CCM1 and CCM2 as critical molecules in Ngbr deficiency–induced endothelial dysfunction and cerebral hemorrhage, and providing what we believe is a new perspective on CCM pathogenesis in the context of HBO1-mediated histone acetylation in preserving the expression of CCM genes. This evidence concerns the gene KAT7 and endothelial dysfunction.