Its sustained activation during inflammation may increase the potential neoplastic transformation of normal cells.17, 31 One proposed mechanism implicates defective IκBα activity and the resulting failure to sequester NF-κB in the cytosol.31 Here we confirmed the increased activation of NF-κB in human colon tumours was correlated with tumour progression. Here, NFKB1 is linked to colonic neoplasm.