Moreover, Calebin A, similar to BMS-345541, reduced the multicellular pro-inflammatory TME-stimulated phosphorylation and translocation of the p65 subunit of NF-κB from the cytoplasm to the nucleus, suggesting that Calebin A, which possesses pro-apoptotic properties, has the potential to prevent tumor invasion and proliferation, at least in part, by up-stream targeting the IKK-NF-κB signaling pathway. Here, NFKB1 is linked to neoplasm.