These results indicate that CEBPB, as the major transcriptional regulator in CEBPB+ GBM subcluster, influences M2 polarization of TAMs by secreting SPP1 that targets the Integrin αvβ1 receptors on TAMs, thereby activating the downstream AKT signaling pathway, and this molecular mechanism directly contributes to a poor prognosis in GBM patients. The gene discussed is SPP1; the disease is glioblastoma.