Larger studies would not only offer a more precise estimate of the APOE ε4-IHD relationship, but also allow the additional study of gene-environment interactions, such as the effects of air pollution, [37] post-traumatic stress syndrome, [38] exercise habits, [39] ultra-processed foods, [40] and other environmental risk factors that may detrimentally synergize with APOE ε4. This evidence concerns the gene APOE and myocardial ischemia.