POUF3F3 drives angiogenesis and tumor expansion, whereas TALC induces M2-macrophage polarization and upregulates the complement components C5/C5a, fostering chemoresistance.440 Other oncogenic lncRNAs, including MALAT1, MEG3, NEAT1, and HOTAIR, promote EMT and contribute to the aggressive phenotype of GBM.441 Moreover, targeting the mTOR pathway to suppress GDEV production offers a potential strategy to disrupt the supportive TME and curb tumor progression.442 Understanding the specific cargo within GDEVs is vital for designing targeted therapies. The gene discussed is C5; the disease is glioblastoma.