Inflammatory bowel disease (IBD) with its two main manifestations Crohn’s disease (CD) and ulcerative colitis (UC) are chronic gastrointestinal disorders with unknown aetiology and no cure (Kaser, 2010). Immunochip experiments have identified about 200 IBD risk loci across the genome (Jostins, 2012, Liu, 2015), which however could only partially explain why IBD has such high heritability, a discrepancy known as ‘missing heritability’ (Zuk, 2012). IBD has dramatically risen in incidence over the last decades in the Western world, and more recently in countries adopting Western lifestyles (Loftus, 2004). Concordance rates in monozygotic twins of 40-50% and 10-15% in CD and UC, respectively, indicate the relative contribution of genetic vs environmental risks (Moller, 2015). This suggests that other than genetic factors might be inherited in IBD pointing at epigenetic alterations (change of DNA methylation). Indeed, intestinal tissues of IBD patients display aberrant DNA methylation profiles compared to healthy individuals (Lin, 2012; Häsler, 2012; Cooke, 2012).