NFKB1 and neoplasm: Constitutive NF-κB and STAT3 activation, often driven by IL-6 within the TME, induces genes for proliferation (e.g., Cyclin D1), survival (e.g., Bcl 2, survivin), angiogenesis (e.g., VEGF), and inflammation, creating feed-forward loops that sustain tumor growth [3].