We envisage that targeting these protein kinases, specifically CDK1/PBK/CHEK1 oncogenic signature, which we identified through in silico analysis, promotes the Gap 2 to mitosis (G2-M) phase cell cycle arrest, apoptosis, and therapy-induced senescence, hence inhibiting GBM progression [20,22,23,24]. The gene discussed is CHEK1; the disease is glioblastoma.