Exemplary, while in a CAC model, IKKβ-dependent activation of NF-κB in myeloid cells promotes tumor growth through the production of IL-6, which stimulates cancer cell proliferation and survival via STAT3 [69,70], we have observed that nuclear accumulation of p50 NF-κB in TAMs supports tumor-promoting inflammation. This evidence concerns the gene NFKB1 and neoplasm.