We provide evidence that BCL-3/NF-κB complexes act as novel activators of the antiapoptotic AKT signalling pathway that has been implicated in the molecular pathogenesis of a variety of human malignancies, including colorectal carcinogenesis.11 As BCL-3 is known to be induced by inflammatory cytokines34, 35 targeting BCL-3 expression (e.g. using non-steroidal anti-inflammatory drugs (NSAIDs)) would not only inhibit a key pathway involved in colorectal tumour progression but could also prevent some of the earliest events in inflamed tissue that drive colorectal tumorigenesis. This evidence concerns the gene BCL3 and colorectal neoplasm.