Monotherapy with vascular endothelial growth factor receptor 2 (VEGFR2) inhibitors shows limited efficacy against glioblastoma multiforme (GBM) in clinical practice, but anti-VEGFR2 therapy can enhance tumor sensitivity to PD-L1 inhibitors by downregulating p21-activated kinase 4 (PAK4) and increasing cytotoxic CD8+ T cell infiltration and activation, providing a novel strategy for combined immunotherapy of GBM (Yao et al., 2025). The gene discussed is CD8A; the disease is glioblastoma.