Specifically, tumor cells educated TANs to overexpress SPP1, GBP1, and ELOVL5, which subsequently activated three key mechanisms: promoting angiogenesis (SPP1-NF-κB-HIF/VEGF), immunosuppression (GBP1-NF-κB-PD-L1), and dysregulated oxidative lipid metabolism (ELOVL5-NF-κB), leading to poor prognosis. The gene discussed is VEGFA; the disease is neoplasm.