This includes autophagy [ATG16L1, IRGM, LRRK2], endoplasmic reticulum stress [XBP1], innate immune cell sensing [NOD2], T cell tolerance [IL10, IL10R], IL23-pathways [IL23R, IL12B], lymphocyte trafficking [CCL7, IL8], and epithelial barrier function [MUC1, MUC3].39–42 Another development in the field of IBD genetics is evidence that genetic associations may be related to disease prognosis in addition to, or instead of, disease susceptibility.43 This might provide a novel avenue to stratify patients and target therapies accordingly. This evidence concerns the gene NOD2 and irritable bowel syndrome.