More specifically, the same mouse model (i.e., atg16l1-/-IEC mice) is susceptible to colitis and enteritis (induced by dextran sodium sulfate colitis or by genetic deletion of Xbp1 (X-box binding protein 1) [18], while protecting against PUFA-induced metabolic enteritis in Gpx4+/-IEC mice, as reported herein. This evidence concerns the gene ATG16L1 and enteritis.