As we previously demonstrated that genetic deletion of Tlr2 and pharmacological blockade of MAPK/JNK signaling contributed to PUFA-induced CXCL1 production and enteritis in this model [6], we tested whether stimulation with the TLR2 agonist Pam2CSK4 was able to induce TLR2 activity in Atg16l1-deficient IECs. Here, ATG16L1 is linked to enteritis.