For example, a statistical interaction among ATG16L1/PTGER4/ZNF300 in CD could imply the involvement of a synergistic combination among autophagy and other possible mechanisms such as immune-inflammation in the etiology of inflammatory bowel disease, which have been repeatedly suggested by genetic studies about their main effects [29-32] as well as mechanistic studies [33,34]. Here, ATG16L1 is linked to Cowden disease.