In adult glioblastomas, the TME is dominated by alternatively activated macrophages, shifting the balance toward immunosuppression.40 These macrophages prevent immune cell recruitment, express high levels of programmed cell death ligand 1 (PD-L1) to suppress T cell activation, and release factors like vascular endothelial growth factor and platelet-derived growth factor to promote angiogenesis and tumor invasion.41,42 However, studies indicate that TAMs function differently in pediatric gliomas than in adults. Here, CD274 is linked to central nervous system cancer.