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 recent meta-analysis concluded that individuals with the G/G or A/G genotypes did have reduced relapse rates compared to A/A individuals, but no difference in abstinence between genotypes was apparent [107]. This pharmacogenetic effect may be explained by differential responses to alcohol based on A118G genotype. Asian Americans carrying the G allele have decreased craving for alcohol when treated with naltrexone, while the medication increases the urge to drink in European Americans with the G allele [116, 117]. Naltrexone also reduces the euphoric effects of alcohol in European Americans with the A/G or G/G genotypes [101]. Confirmation of these findings, preferably taking into account potential ethnic differences, would help further explain the effect of A118G genotype on alcoholism treatment. While numerous pharmacogenetic studies have examined the role of A118G in naltrexone treatment, the amount of research on the interaction between OPRM1 genotype and other treatments is extremely limited. A single clinical trial showed no effect of two OPRM1 SNPs, including A118G,
