These TAMs exhibited down-regulation of the microglia core signature and concomitant up-regulation of inflammatory, metabolic, and hypoxia-related genes, including SPP1, and several type I interferon genes, APOE, and CD163. Furthermore, the top differentially expressed proteins, including HLA-DR, TREM2, APOE, CD163, and GPR56, could be detected in a TAM subset via CyTOF, providing a possibility for therapeutically targeting specific TAM states in GBM (75). The gene discussed is CD163; the disease is glioblastoma.