In NSCLC, AA downregulated the TNF-α induced activation of IKKβ, IkB and blocked the NF-kB nuclear translocation dose-dependently. AA directly bound to IKKβ, while its binding with IKKα was much lower, suggesting specificity for IKKβ. In addition, AA downregulated the proliferation (VEGF, IGFR1, TGF-β) and oncogenic genes (C-myc and NF-κB), and increased levels of antioxidants. This evidence concerns the gene NFKB1 and non-small cell lung carcinoma.