Human laboratory studies have identified that carriers of the G allele have increased subjective alcohol effects (Ray & Hutchison, 2004), stronger cue-induced craving (van den Wildenberg et al., 2007) and stronger automatic approach tendencies toward alcohol and other appetitive stimuli (Wiers et al., 2009). Moreover, these various facets of alcohol approach motivation and reward such as alcohol stimulation, positive mood, craving and enjoyment are blunted by naltrexone, particularly for those with the G allele (Ray & Hutchison, 2007). It is therefore of considerable interest that seemingly consilient findings can be observed in nonhuman animals. For example, deletion of the mu opioid receptor gene in mice abolishes ethanol drinking (Roberts et al., 2000) and reduces motor impulsivity and the enhancement of motor impulsivity by ethanol (Olmstead et al., 2009). In primates, carriers of a functionally equivalent variant of the mu-opioid receptor had higher alcohol preference that naltrexone reduced providing additional evidence supporting the therapeutic potential of naltrexone. Efforts such as these that work across human and animal studies to examine how genes modify responses to pharmacological agents may ultimately inform our
