Cardiovascular disease is associated with nonmodifiable risk factors such as age, gender, and genetic background, and with modifiable risk factors such as lipid concentrations. Lowering serum lipid levels has been demonstrated to slow the progression of, or even induce regression in, atherosclerosis. However, like any other drug treatment, the magnitude of plasma lipid responses to drug therapies varies considerably among individuals. Pharmacogenetics provides the experimental basis to understand the variability in response to drugs as a function of the individual genetic makeup. Information from small clinical trials reveals that several candidate genes may hold some promise in our quest to predict individual success to hypolipemic drug treatment. However, the current clinical relevance of this knowledge is quite limited due to the small effects observed for each of the genetic markers examined. Future progress in this area will be driven by studying gene-gene and gene-treatment interactions in much larger patient populations.