These studies indicated that induction of TLR2 activity with a prototypical TLR2 ligand (Pam2CSK4) evoked CXCL1 production in Atg16l1-deficient IECs and enteritis in our model, suggesting that ATG16L1 controlled TLR2 activity upstream of this receptor while being dispensable for execution of TLR2 (downstream) signaling. Here, ATG16L1 is linked to enteritis.