Using our GBM-on-a-Chip model, we demonstrated that M2-like CD68+CD163+ TAMs dominated the immunosuppressive microenvironment in the MES GBM, by restricting the dynamics of CD8+ T-cell recruitment and activation, which can be effectively reversed with CSF-1R and PD-1 dual blockade therapy. This evidence concerns the gene PDCD1 and glioblastoma.