Although it has been reported that NF–κB signaling in gastric epithelial cells may protect against H. felis-induced gastritis and the subsequent development of dysplasia [147], our group has suggested that NF–κB activation in gastric epithelial cells promotes gastric carcinogenesis via IL-1α production in a chemically induced mouse tumor model [148]. This evidence concerns the gene NFKB1 and gastritis.