Examining the data from the current study along with the data derived from prior association and sequencing studies suggests that at a minimum, there currently is strong evidence of association to causal variation in IBD (i.e. missense, nonsense or splice junction variants) in the NOD2, ATG16L1, IL23R, MST1, CARD9, IL18RAP and RNF186 genes, and at least suggestive evidence for causal variation in the CUL2, C1orf106, PTPN22, MUC19, CEP72, LAMB1, CCR6, JAK2, and STAC2 genes (Current study and references [4], [5], [7], [11], [31]). This evidence concerns the gene ATG16L1 and inflammatory bowel disease.