In the top 500 regulated transcripts, we demonstrate that only in IL-22–treated Atg16l1ΔIEC, but not Atg16l1fl/fl organoids, a significant enrichment of up-regulated processes related to innate immunity, herpes simplex infection, and cellular response to IFN-β is present in addition to expected pathways (e.g., ER stress and NF-κB activation; Fig. 2 C). This evidence concerns the gene NFKB1 and herpes simplex infectious disease.