These findings provide insights into the molecular mechanisms underlying the synergistic effects, suggesting potential biomarkers, such as alterations in the expression of EZH2 and CDK4/6, MGMT promoter methylation status, activity levels of signaling pathways (e.g., Wnt/β-Catenin and PI3K/Akt), expression of mitotic genes (e.g., Rb, PLK1, TPX2), DNA repair genes (e.g., EXO1 and CKAP2L), and changes in stemness markers (e.g., NANOG and OCT3/4) toward a more differentiated state, ultimately influencing GBM invasiveness. The gene discussed is PLK1; the disease is glioblastoma.