Cessation treatment may be improved via personalized medicine: i.e., using individual genetic markers to maximize efficacy and minimize side effects (McMahon and Insel, 2012; Vaidyanathan, 2012). Smokers vary greatly in the benefit they derive from particular pharmacotherapies, and genotypes may predict their response to a specific pharmacotherapy (Chen et al., 2014; David et al., 2013; Gold and Lerman, 2012; McGeary et al., 2012; Ray et al., 2009; Rose et al., 2010; Uhl et al., 2010). Large scale genome-wide association (GWA) meta-analyses (Liu et al., 2010; TAG, 2010; Thorgeirsson et al., 2010) have confirmed an association between nicotine dependence and the genetic variant rs16969968, which results in an amino acid change (D398N) in the nicotinic receptor gene CHRNA5 (Saccone et al., 2007). CHRNA5 encodes the α5 nicotinic receptor subunit and plays a role in the pharmacodynamic pathway of nicotine dependence (Fowler et al., 2011). Further studies have demonstrated change in the receptor function in response to nicotine agonists given this amino acid change in the a5 nicotinic receptor subunit (Bierut et al., 2008a; Brown et al., 2007). Growing evidence indicates that
