In the DEN model, where inhibition of IKKβ/NF-κB signaling in hepatocytes was shown to promote HCC development, additional deletion of IKKβ in liver myeloid cells diminished the production of proinflammatory cytokines, reduced liver compensatory proliferation, and strongly inhibited DEN-induced hepatocarcinogenesis.63 The activation of NF-κB in the myeloid cells was shown to be dependent on the release of IL-1α by the dying hepatocytes.69 Moreover, NF-κB apparently polarizes macrophages toward the alternatively activated M2 phenotype, which are tumor-promoting and immunosuppressive.70 This evidence concerns the gene IL1A and neoplasm.