In the twentieth century, coronary artery disease (CAD) was the major cause of morbidity and mortality in western societies. Genetics and environmental influences clearly contribute to CAD. Our genetic makeup contributes to not only coronary risk factors, but also determines an individual's response to environmental challenges such as diet, drugs, and tobacco. Genetic testing is likely to be more predictive of our predisposition to CAD than current conventional testing of known risk factors. Therapy aimed at altering the regulation of genes or their transcribed proteins may prove appropriate in individual patients, depending on their genetic background. The understanding of our genetic predisposition to CAD may enable targeted environmental modification strategies aimed at individuals at greatest risk. Both in terms of the huge costs of drugs to society and in terms of needless medicalization, genotyping in order to tailor therapy might become a routine part of risk management earlier than we think.