Mechanistically, CSF1/IL-34–CSF1R activates PI3K/Akt–mTOR and ERK in macrophages, enforcing an FAO/OXPHOS-biased, IRF4/PPARγ program that raises IL-10, VEGF-A, and PD-L1 while suppressing antigen presentation—thereby promoting angiogenesis and limiting cytotoxic immunity [44]; glioblastoma stem cells supply CSF1/IL-34 and trophic cues that stabilize these CSF1R-dependent states in perivascular/hypoxic niches. The gene discussed is CSF1; the disease is glioblastoma.