Although it is tempting to interpret the estimate for CHD seen in non-smoking ε4 carriers as suggestive that this subgroup does not have an elevated risk of CHD compared to non-ε4 carriers (since the 95%CI includes the null), this is likely due to reduced power within strata of subgroups, and the salient feature is the lack of evidence for interaction between APOE genotype and smoking status. This evidence concerns the gene APOE and coronary artery disorder.