Given that activation of the transcription factor NF-κB signaling cascade mediates the stimulation of the proinflammatory TME in CRC, we sought to examine if Calebin A had the potential in inhibiting TME-promoted NF-κB activation and NF-κB-promoted gene products involved in proliferation (Ki-67), invasion (MMP-9), metastasis (CXCR4, β1-integrin), and apoptosis (cleavage of Caspase-3). This evidence concerns the gene NFKB1 and colorectal carcinoma.