Interestingly, TP53 mutations are also able to generate an inflammatory response in their own right through oncogenic “gain-of-function” effects (104): human organoid studies and in vivo studies in p53mut/+ mice demonstrate that epithelial cells bearing a p53 mutation commonly observed in IBD (R273H) can exacerbate their local inflammatory microenvironment, by prolonging TNFα-induced NFκB activation, eventually generating flat dysplastic lesions with secondary cancers typical of those seen in IBD (105). This evidence concerns the gene NFKB1 and inflammatory bowel disease.