Numerous risk loci have been reported for alcohol dependence by the candidate gene approach. Most of these risk genes implicated have been from (1) classical neurotransmitter signaling systems, including the dopaminergic (e.g., MAOA, COMT, and NCAM1-TTC12-ANKK1-DRD2; Bau et al., 2001; Hutchison et al., 2002; Dick and Foroud, 2003; Olsson et al., 2004; Dahmen et al., 2005; Kohnke et al., 2005; Gelernter et al., 2006; Stapleton et al., 2007; Huang et al., 2008; Yang et al., 2008), serotoninergic (e.g., SLC6A4 and HTR2B), GABAergic (e.g., GABRA2 and GABRG1), and cholinergic systems (e.g., CHRM2 and CHRNA5-CHRNA3-CHRNB4); (2) non-classical neurotransmitter signaling systems (e.g., CRHR1); (3) the ethanol metabolic pathway (e.g., ADH1B, ADH1C, ADH4 and ALDH2; Luo et al., 2006b; Uhl et al., 2008); and (4) the opioidergic signaling pathway (e.g., OPRM1, OPRD1 and OPRK1; Gelernter and Kranzler, 2009; Ray et al., 2006; Zhang et al., 2006). In recent years, genome-wide association studies (GWASs; Treutlein et al., 2009; Bierut et al., 2010; Edenberg et al., 2010; Heath et al., 2011) also reported risk loci for alcohol dependence (summarized previously in Zuo et al., 2012). In
