Alcohol consumption and problems are complex human behaviors that are influenced by both genetic and environmental risk factors (Kendler et al., 1992; Kendler et al., 1994). One strong candidate gene for alcohol-related outcomes is the dopamine receptor D2 gene (DRD2). In 1989, it was hypothesized that the rewarding effects of alcohol are mediated through the mesolimbic dopamine system (Wise and Rompre, 1989). The association between DRD2 and alcoholism was first reported by Blum and colleagues, who found that an increased frequency of the Taq1A1 restriction fragment length polymorphism was observed in postmortem brain tissue from alcoholics (as compared to nonalcoholic controls) (Blum et al., 1990). Since this initial report, there has been an extensive literature examining the relationship between DRD2 and alcohol-related outcomes. While there have been subsequent replications of this genetic association (Blum et al., 1991; Comings et al., 1991; Parsian et al., 1991; Amadeo et al., 1993; Noble et al., 1994; Higuchi et al., 1994; Neiswanger et al., 1995; Hietala et al., 1997; Kono et al., 1997; Ishiguro et al., 1998; Noble, 2003; Foley et al., 2004; Konishi
