Studies have suggested that blockade of CDK1 induces synthetic lethality in malignant gliomas25; moreover, FoxM1 promotes β-catenin nuclear localization and controls Wnt target gene expression and glioma tumorigenesis26; ID2 promotes the survival of glioblastoma cells during metabolic stress by regulating mitochondrial function27. Here, CDK1 is linked to glioblastoma.