“…Finally, GWAS has identified genomic loci not involved in coding for nAChR subunits that may play a role in risk of tobacco dependence and as such may be suitable for the development of novel therapeutics. For example, polymorphisms in the galanin 1 receptor (Lori et al, 2011), 5-HT2A and 2C receptors (Iordanidou et al, 2010;Polina, Contini, Hutz, & Bau, 2009;White, Young, Morris, & Lawford, 2011), neuropeptide Y (NPY), Y2 receptor (Sato et al, 2010), catechol-O-methyltransferase (COMT) (Nedic et al, 2010), Rho GTPases (Chen et al, 2007;Lind et al, 2010), muscarinic receptors 2 and 5 (Anney et al, 2007;Mobascher et al, 2010), brain-derived neurotropic factor and its receptor (TrkB) (Amos, Spitz, & Cinciripini, 2010; "Genomewide meta-analyses identify multiple loci associated with smoking behavior, " 2010; Li, Lou, Chen, Ma, & Elston, 2008;Vink et al, 2009), neuroexin-1 (Nussbaum et al, 2008), CYP2A6 and CYP2B6 (Nakajima, 2007;Ring et al, 2007;Sellers, Tyndale, & Fernandes, 2003;Thorgeirsson et al, 2010), β-arrestin 1 and 2 (Sun, Ma, Payne, & Li, 2008), phosphatase and tensin homolog gene (Zhang, Kendler, & Chen, 2006), and GABA-B receptors (Li et al, 2009) are all associated with nicotine dependence. These findings suggest that observations made in the human genetics literature identifying genes influencing vulnerability to tobacco dependence may be leveraged for future medications development.…”