Finally, given that our CADASIL hBVO model exhibited known NOTCH3 signaling-driven vasculopathies, such as actin filament node formation, increased apoptosis, mural cell degeneration, and impaired endothelial-mural cell connections, it will serve as a valuable research platform for investigating CADASIL pathogenesis and conducting drug screening. This evidence concerns the gene NOTCH3 and vascular disorder.