The discovery of a connection between TCF21, one of the most highly replicated GWAS candidate genes for coronary artery disease, and AHR, a gene classically involved with response to environmental toxins raises an interesting hypothesis that this interaction may reflect gene-environment interactions that are contributing to CAD and presents an opportunity to define causal gene-gene and gene-environment interactions relevant to the atherosclerotic lesion. This evidence concerns the gene AHR and coronary artery disorder.