This process, resembling IL-1β secretion [31], involves lysosomal damage and dynamic autophagic flux, suggesting that extracellular ENO1 remodels the TME through paracrine signaling to drive metabolic reprogramming in neighboring tumor or immune cells, thereby contributing to GBM malignancy, fostering immune evasion, and potentially mediating resistance to TMZ. The gene discussed is IL1B; the disease is neoplasm.