Cancer metabolism consists of highly interconnected and intricately regulated pathways, often resulting in compensatory mechanisms.[48] GBM cells with high GS expression synthesize glutamine for their own use, while those with low GS expression rely on glutamine acquisition from surrounding astrocytes.[11] Consequently, targeting HDAC6 or USP9X to reduce GS expression may induce compensatory mechanisms such as upregulation of glutamine transporters. Here, GLUL is linked to glioblastoma.