CD8A and neoplasm: This suggests the possibility that the anti-VEGF treatment promotes the infiltration of CD8+ T cells activated by anti-PD-L1 into the tumor by enhancing the expression of vascular endothelial adhesion molecules and through the production of chemokines, also in the metastatic brain tumor. Further research will be required to understand the detailed mechanism for why the number of CD8+ T cells increased in the brain metastasis model.