the likelihood of developing a drinking problem (Chai et al., 2005; Edenberg et al., 2006; Macgregor et al., 2009; Tolstrup et al., 2008). Human genetic studies have similarly identified alcoholism candidate genes involving neurotransmitter pathways associated with brain reward processes including the dopaminergic (e.g., DRD2, MAOA, COMT), serotoninergic (e.g., HTR3A, HTR1B, HTR3B), GABAergic (e.g., GABRA1, GABRA2), glutaminergic (GAD1, GRIK3, GRIN2C) and opioid (e.g., OPRM1, OPRD1; Blum et al., 1990; Bolos et al., 1990; Edenberg, 2012; Edenberg and Foroud, 2013; Edenberg et al., 2008; Feinn et al., 2005; Luo et al., 2005; Radel et al., 2005; Zhang et al., 2008). These genes presumably directly impact the reinforcing properties of alcohol driving the motivation to seek and use alcohol to excess. Whole-genome studies have shown abnormalities of chromosomes and identified specific regions (e.g., 4p12, 7q31.32, 13q14.2) where known or candidate genes for alcoholism are located and for alcoholism-related phenotypes such as age of drinking onset (3q26.1, 5q11.2, and 12q32.2; Edenberg, 2012; Edenberg and Foroud, 2013; Enoch, 2013; Kapoor et al., 2014; Morozova et al., 2014; Radel et al., 2005; Yan et al., 2014).
