Deletion of NF-κB1 has been shown to protect from allergic airway inflammation,24 whereas NF-κB1ΔC/ΔC mice, which constitutively overexpress transcriptionally active NF-κB1 p50, develop spontaneous hepatic and pulmonary inflammation in standard conditions.25 Conversely, colitis induced by intragastric administration of Helicobacter hepaticus was more severe in Nfkb1−/− mice than WT,26 which is concordant with our observation of spontaneous gastric inflammation in mice of this genotype. This evidence concerns the gene NFKB1 and colitis.