As expected, KD of HELDR or KAT7 markedly decreased while KAT7 overexpression rescued the enrichment of KAT7, H3K14ac, and H4K12ac at the promoters of these genes in GSCs (Fig. 6k–m, Extended data Fig. 6l–o), Together, these results indicate that the KAT7-H3K14ac/H4K12ac axis is a critical downstream mediator for HELDR-regulated GBM tumorigenic properties. This evidence concerns the gene KAT7 and glioblastoma.