Using a mouse model with genetically color-coded MΦ (Ccr2RFP) and MG (Cx3cr1GFP), they showed that even in mice lacking Ccr2-mediated MΦ recruitment to the brain (Ccr2RFP/RFPCx3cr1GFP/+), MG-mediated GBM phagocytosis was sufficient to reduce tumor burden and prolong survival under anti-CD47 treatment. This evidence concerns the gene CCR2 and glioblastoma.