Crucially, tumor-specific knockdown of <i>SLC1A3</i> dismantled this vascular-immune suppressive niche, significantly restoring T cell activation in a multicellular co-culture model.<h4>Discussion</h4>Our findings establish SLC1A3 not merely as an intrinsic driver of glioma development, but as a critical upstream node orchestrating a cascading tumor-endothelial-T cell immunosuppressive axis. This evidence concerns the gene SLC1A3 and neoplasm.