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. The gene discussed is CD274; the disease is glioblastoma.