Moreover, RNA sequencing and lipidomic profiling of PUFA-exposed IECs indicate that ATG16L1 is required for PTGS2/COX2 expression and prostanoid formation, which likely exert inflammatory actions [31], and PTGS2/COX2-related lipid mediators are thought to contribute to intestinal inflammation in IBD [32]. This evidence concerns the gene ATG16L1 and inflammatory bowel disease.