To further demonstrate whether CDK5-promoted TRIM59 nuclear translocation is critical for glioma tumorigenicity, we analyzed the effects of EGFR inhibitor erlotinib and CDK5 inhibitor Roscovitine treatments on patient-derived glioma stem-like cells (GSCs) and primary GBM cells using established methods to evaluate cell signaling pathways, self-renewal, and tumor-forming ability47,48. The gene discussed is TRIM59; the disease is glioblastoma.