Intestinal epithelial barrier dysfunction is considered as a risk factor in the pathogenesis of Crohn’s disease (CD), and since there is no FDA approved therapy available, there is a need for identifying a relevant model to study and test therapies to correct this defect. Previously, we demonstrated that inflammatory environment of CD affects properties of intestinal stem cell (ISC) niche, ablating its ability to form enteroids (EnOs) in our mouse model for CD-like ileitis (SAMP/YitFc, SAMP) (doi.org/10.1016/S0016-5085(17)32213-8).