Oslin et al. originally identified an association between A118G allele and naltrexone response (Table 2) [106]. Patients carrying the G allele had lower rates of relapse to heavy drinking on naltrexone than those with the A/A genotype; however, no difference in abstinence rates was observed between the genotypic groups [106]. Both the findings in relapse rates and abstinence rates were replicated in a Korean cohort [109]. Other studies have also demonstrated that naltrexone is more effective in reducing heavy drinking in individuals carrying the G allele [110, 111]. Two additional trials found no association at all between A118G and naltrexone efficacy, while a third trial found no association for either A118G or rs648893 [112-114]. Another study suggested that naltrexone reduced heavy drinking only in patients who had both the A/A genotype at A118G and the nine copy variant of the variable number tandem repeat (VNTR) in the dopamine transporter gene (DAT1) [115]. The inability of these studies to replicate the original association between A118G and naltrexone efficacy may be partially attributed to differences in patient demographics or outcome measurements. A
