Various subtypes of GBM exhibited diverse CD8+ T-cell dynamics, and a CSF-1R inhibitor could enhance the efficacy of the PD-1 inhibitor, revealing that immunotherapeutic efficacy for GBM may be improved by immune checkpoint inhibitors targeting PD-1 combined with inhibitors targeting TAM-associated CSF-1R signalling (Figures 7Bii, iii). The gene discussed is PDCD1; the disease is glioblastoma.