In summary, we confirm that HEY1 is overexpressed in the GBM condition; DNMT1's reduced activity might lead to hypomethylation of the HEY1 promoter sequence, causing constitutive expression of HEY1 and mutant p53; and therapies that inactivate HEY1 via transcriptional interference or methylation of the CpG island-rich promoter sequence show promise in reducing the cancer phenotype. Here, TP53 is linked to glioblastoma.