ATG16L1 and Crohn disease: NOD2‐ and ATG16L1‐mediated autophagies are required for DCs to process and present bacteria antigen via major histocompatibility complex (MHC) class II and I to induce CD4 and CD8 T‐cell response.37 Individuals carrying NOD2 and ATG16L1 polymorphisms display impaired antigen presentation in mucosal DCs and are at increased risk of developing Crohn's disease.38, 39 XBP1 is constitutively spliced in DCs, highlighting the importance of consistent UPR activation.