Use of tobacco is the single greatest preventable cause of death in the USA, with a substantial impact on morbidity and mortality worldwide. One in five Americans is a current smoker, and available therapies are efficacious for only a small fraction of those who attempt to quit (1). Bupropion, an anti-depressant therapy, is among the only two FDA-approved non-nicotine pharmacotherapies available for the treatment of nicotine dependence. While its efficacy is well-documented, there is substantial inter-individual variability in therapeutic response (2–4), and most smokers do not maintain long-term abstinence (5,6). Pharmacogenetic studies may improve the outcomes of bupropion therapy for smoking cessation by identifying smokers most and least likely to benefit based on inherited differences in drug metabolism and CNS targets. Such studies may also identify genetic markers of relapse risk, thereby identifying smokers who may require more intensive treatment.
