Finally, the proposed tumor-endothelial-T cell multi-cellular axis was functionally validated utilizing <i>in vitro</i> tumor-HUVEC co-culture systems, qPCR, and FACS-based T cell activation (NFAT-Jurkat) assays.<h4>Results</h4>Our multi-omics re-analysis identified extensive alternative splicing and transcriptional reprogramming during GICs evolution, pinpointing SLC1A3 as a core gene significantly upregulated along the malignant pseudotime trajectory and strongly correlated with poor clinical prognosis in GBM. The gene discussed is SLC1A3; the disease is neoplasm.