In conclusion, the present study provides evidence in support of an interaction model of the role of CNR1 in the risk for CD in EAs. SNP8 locus may be implicated in CIP as well. CNR1 could also play a role in the risk for CD in AAs. The two loci could ultimately be relevant to research on the prevention and treatment of CD. Further studies are warranted to replicate the findings in the present study, to locate the causal variants around SNP3 and SNP8 that contribute to risk of CD and to uncover the mechanism by which these two independent loci modulate that risk.
