Crohn’s disease is a chronic heterogenous disorder with patients showing complex phenotypes and highly variable response to therapies. GWAS studies have identified hundreds of genetic factors associated with the disease but the precise mechanism with which these genes cause variable phenotype in the disease are unknown. We observed an autosomal analog of X-chromosome inactivation causes clonally stable epigenetic mosaicism in intestinal organoids generated from mice. This epigenetic mosaicism was detected by measuring allele specific expression in organoids grown from different individuals and from spatially different regions of the mouse intestine.