This is due to the roles of aberrant activation of Notch components in GBM, such as overexpression of DLL-4 and JAG-1 were detected in GBM endothelial cells and promoted the maintenance and differentiation of glioma stem cells via activating the down-stream Hes1 in tumor cells (Zheng et al., 2021). This evidence concerns the gene HES1 and glioblastoma.