To this end, we exploited a well-characterized mouse model for CD, i.e., SAMP1/YitFc (SAMP), in which the main pathology is a spontaneous ileitis that is strikingly similar to human CD, with skip lesions, transmural inflammation, and scarring that can lead to stricture formation (47, 48). This evidence concerns the gene XPNPEP1 and Crohn ileitis.