Identification of high impact SNPs in NOD2 that are associated with adult Crohn's disease with clear involvement in IBD pathogenesis has illustrated a genetic continuum between adult and early‐onset IBD, in contrast to the classical view of two genetically independent diseases.24 In this context, we can hypothesize that adult and Mendelian IBD arise as a result of a spectrum of varyingly pathogenic genetic lesions that impact common key pathways in IBD. The gene discussed is NOD2; the disease is inflammatory bowel disease.