Recently, it has been indicated in Rorα-deficient and Rorαsg/sg/Rag1−/− mouse models that the Rorα-dependent ILC3, rather than ILC2, function in the development of intestinal fibrosis, hinting at a potential therapeutic target for IBD31. Here, RORA is linked to inflammatory bowel disease (infantile ulcerative colitis) 31, autosomal recessive.