When transgenic mice lacking specific NF-κB subunits were subjected to dextran sulphate sodium (DSS) treatment in a model of colitis, mice lacking cRel and Nfkb1 developed more severe colitis than wild-type controls, whereas Nfkb2−/− mice were resistant to colitis (Burkitt et al., 2015). This evidence concerns the gene NFKB2 and colitis.