The identification of GPNMB as the key factor mediating TAM-GSC bidirectional communication, combined with our findings showing antitumor effects resulting from TAM depletion of GPNMB in GBM mouse models, indicates an effective therapeutic intervention strategy of targeting TAM-GSC bidirectional communication and encourages the development of therapeutic agents targeting GPNMB-expressing TAMs in patients with GBM. This evidence concerns the gene GPNMB and glioblastoma.