Among the 163 genome-wide significant IBD susceptibility loci as identified in the study by Jostins et al. (4), genetic variants in immune system components (NOD2, IL-23R, IL-12B, JAK2, and FUT2) and autophagy [ATG16L1, leucine-rich repeat kinase 2 (LRRK2)] could (jointly) contribute to the activation of mesenchymal cells and pathogenesis of fibrosis (4, 9, 133). This evidence concerns the gene ATG16L1 and inflammatory bowel disease.