In IBD, previous studies reported that knocking out autophagy-related key genes, including Atg4B/autophagin-1, Atg16L1, and activating transcription factor 4 (ATF4) significantly deteriorated the severity of IBD in animal models, suggesting that baseline autophagy was vital for the maintenance of intestinal homeostasis and the function of the intestinal defensive barrier36–39. This evidence concerns the gene ATG16L1 and inflammatory bowel disease.