However, the presence of a functional CDT promoted an enhanced inflammatory response at 4 months post-infection, prior the development of the dysplasia, characterized by enhanced transcription of NFκB subunits p50 and p65, and pro-the inflammatory mediators TNFα, IL-6, IFNγ, Cox-2, and anti-apoptotic Bcl-2 and Bcl-X(L) effectors in mice infected with the genotoxigenic H. hepaticus compared to mice infected with the control cdtB deficient strain [31]. Here, NFKB1 is linked to infection.