To achieve this goal, we assessed the impact of the NF-κB inhibitor, BAY 11–7082, and the IκBα super-repressor, IκBαSR, a dominant-negative mutant of IκBα (Wu et al., 2015), which blocks the effects of NF-κB activation on the viability and clonogenicity of CRC cells. This evidence concerns the gene NFKBIA and colorectal carcinoma.