In support of this concept, deletion of the NF-kB activator, IkB kinase β (IKKβ), specifically in IEC (IKKβIEC−/−), does not prevent dextran sodium sulfate (DSS)-induced colitis [36], and mice selectively defective in IEC for the main IKK subunit, IKKγ (IKKγIEC−/−), spontaneously develop colitis [37]. This evidence concerns the gene NFKB1 and colitis.