ATG16L1 and colitis: In a DSS-induced colitis model, stimulation of colonocytes with TNFα and NOD ligands promotes IKKα to phosphorylate ATG16L1 (Ser278), stabilising ATG16L1 against degradation, which is associated with protection against IREα-mediated ER stress and activation of caspase-12, which causes a loss of cytoprotective IL-18 [99].