Deletion of Atg16L1 increases the production of IL-1β and IL-18 in macrophages in response to LPS, and mice lacking Atg16L1 are more susceptible to dextran sulfate sodium-induced colitis.63 Atg16L1-deficient dendritic cells fail to induce regulatory T cells to suppress mucosal inflammation.65 Pharmacological inhibition of autophagy was reported to up-regulate the expression of IL-23 in cultured macrophages,66 but it remains unclear if such regulation has any role in intestinal fibrosis. The gene discussed is ATG16L1; the disease is colitis.