It is of interest that activated AKT also phosphorylates IκB kinase (IKK), to directly activate NF-κB signalling.55 Indeed, crosstalk between AKT and NF-κB signalling has already been shown to promote cell survival.55, 56 Here we present a novel mechanism by which AKT activity can be increased in colorectal epithelial cells; our results suggest that potentiation of AKT signalling (observed in both adenoma-derived RG/C2 and five carcinoma-derived cell lines) is central to the pro-tumorigenic role of BCL-3. The gene discussed is AKT1; the disease is adenoma.