The results further showed that Calebin A could significantly increase all above-mentioned effects in both CRC cells to 5-FU at least in part by suppression of master pro-inflammatory transcription factor, NF-κB and pro-inflammatory agents that are linked with tumor growth by the activation of genes coding for NF-κB-mediated anti-apoptotic and pro-proliferation molecules in the tumor environment. This evidence concerns the gene NFKB1 and neoplasm.