Paneth cells are the functional foreground where IBD-associated genetic mutations (such as NOD2, ATG16L1, or XBP1) manifest their phenotypic consequences.82–86 Apart from allowing increased epithelial access to luminal pathogens, an altered Paneth cell functional profile also suggests a decrease in epithelial Wnt and Notch signaling, sided with a deficiency of growth factors required for stem cell proliferation and differentiation. Here, ATG16L1 is linked to inflammatory bowel disease.