The reasons could be: 1) variants in NOD2 have shown strong preference to CD versus UC, while other loci including MHC could play roles in both CD and UC with a weaker preference; 2) NOD2 is among the most powered IBD associated loci, allowing a comprehensive set of the causal variants to be fine-mapped (ten causal variants in this study). The gene discussed is NOD2; the disease is inflammatory bowel disease.