E2F propagates key genes involved in cell cycle acceleration, DNA replication and mitotic progression.3 Genetic alterations in the CDK4/6 proteins and RB1 are reportedly involved in over 78% of GBM, with prominence in the classical and mesenchymal subtypes of GBM.4 Amplification of CDK6 and deletion of the cyclin-dependent kinase inhibitor 2A/B (CDKN2A/B) genes are frequently reported aberrations in primary GBM.5 This evidence concerns the gene CDK4 and glioblastoma.