We have previously described an innate model of IBD that occurs spontaneously in the absence of adaptive immunity, is early onset, and 100% penetrant.1 Specifically, mice expressing TNFAIP3 (A20) in intestinal epithelial cells (villin-TNFAIP3 mice) crossed to RAG1−/− mice (villin-TNFAIP3 x RAG1−/− mice; aka TRAG mice) spontaneously develop colitis that is not observed in villin-TNFAIP3 or RAG1−/− littermates.1 We have explored the colitis in TRAG mice to better understand contributions of innate immunity to IBD. The gene discussed is RAG1; the disease is inflammatory bowel disease.