Interestingly, treatment with Calebin A lowered the nuclear staining and nuclear translocation of p65-NF-κB in CRC cells in a dose-dependent manner (1, 2, and 5 μM) in both multicellular proinflammatory TME cultures (85%, 37%, and 21%) and in TNF-β-TME (76%, 30%, and 22%), respectively, suggesting the essential synergistic role of the paracrine interaction between HCT116, MRC-5 cells, and T-lymphocytes/TNF-β in maintaining tumor promotion. The gene discussed is NFKB1; the disease is colorectal carcinoma.