GWAS identified Atg16L1 and immune-associated GTPase M (IRGM) deletions in CD, and Atg16L1 gene deletionin bone marrow chimeric mice resulted in excessive IL-1β production by macrophages (126), and altered expression of IRGM resulted in defective autophagy in CD (127), which is related to the pathogenesis of CD and may be one of the etiological factors of IBD. The gene discussed is IL1B; the disease is inflammatory bowel disease.