Although the regulatory effect of the NOD2-ATG16L1 pathway on autophagy has been widely studied in IBD (Brain et al. 2010; Travassos et al. 2010; Wang et al. 2014; Hu and Peter 2013), to determine whether the regulation of autophagy by NOD2 mainly comes from ATG16L1, we needed a depletion experiment to determine whether NOD2 participates in autophagic regulation through pathways other than ATG16L1. This evidence concerns the gene ATG16L1 and inflammatory bowel disease.