Beyond recruitment and maintenance, specific contact and soluble interactions impose immune suppression and invasion: SPP1–CD44 signaling is upregulated in glioblastoma and integrates with STAT3/CEBP-β-driven programs to promote immunoregulatory TAM phenotypes and tumor aggressiveness (21–23); TGF-β signaling further enforces antigen-presentation deficits and exclusionary stromal remodeling; the CD47–SIRPα axis inhibits macrophage phagocytosis; and PD-L1–PD-1 engagement dampens T-cell effector function within TAM-dense niches. The gene discussed is CD47; the disease is neoplasm.