Once an individual is addicted, the current clinical options for treatment are rather limited and only partially effective. Current pharmacotherapies and behavioral counseling improves the likelihood of smoking cessation by approximately 1.5 to 2.0 fold, with high rates of relapse and an average of 4–5 quit attempts needed before success (50). Personalized medication choices can be facilitated to a great extent by genetic studies, and provide novel insights into pharmacodynamics, pharmacokinetics and other aspects of the disposition of medications. Pharmacogenetic studies have already identified individuals that respond better to certain types of therapies for drug addiction based on their genetic makeup (Table 3). For example, functional variation in DBH, DRD2, OPRM1, CYP2A6 and CYP2B6 has been associated with smoking abstinence rates in clinical trials, either in response to pharmacotherapy or placebo (reviewed in (4), Supplementary table 4), although not always consistently. Other pharmacogenetic studies have examined treatment response for alcohol or opiate dependence. Variability in genes that are involved in methadone metabolism, such as CYP3A4 and CYP2D6, as well as genetic variation in P-glycoprotein (ABCB1, MDR1), for which methadone is
