These range from almost exclusively genetically driven disease (e.g., monogenic forms of IBD, such as those associated with mutations in IL10RA/B or the X-linked inhibitor of apoptosis (XIAP) [3] and entities with a large genetic contribution such as very early onset (VEO)-IBD) [4], to phenotypes that are more dependent on environmental factors. The gene discussed is XIAP; the disease is inflammatory bowel disease.