IBD patients with the ATG16L1 and NOD2 mutations, as well as studies on murine models have demonstrated the disturbed secretory apparatus of P cells, resulting in defects of antibacterial autophagy [218]; (b) non-coding RNA regulators and their polymorphisms in combination with epigenetic factors (as discussed in Section 6 and Table S2) alter gene regulation; and (c) specific ncRNA actions, such as the miR-31 binding potential on cytokine receptors, are crucial to inflammation control, as found in DSS-induced colitis [219]. This evidence concerns the gene ATG16L1 and colitis.