Likewise, results of behavioral/laboratory studies of naltrexone pharmacogenetics have not been completely consistent. For instance, a placebo-controlled study of nontreatment seekers found that Asp40 carriers treated with naltrexone reported greater cue-induced craving for alcohol, than Asn40 homozygotes, and as compared to placebo (McGeary et al., 2006). Further analyses of the same sample failed to support a pharmacogenetic effect on measures of alcohol use and urge to drink in the natural environment, using EMA (Tidey et al., 2008). Similar null findings were reported for measures of cue-reactivity in a mixed sample comprised of both nontreatment-seeking and treatment-seeking alcohol-dependent individuals (Ooteman et al., 2009). A small neuroimaging study examined the pharmacogenetics of naltrexone on delay discounting (n = 19) and did not support the pharmacogenetic effect of the Asn40Asp SNP of OPRM1 on impulsive decision-making as well as activation of its underlying neurocircuitry (Boettiger et al., 2009). Such null findings highlight the need to cautiously evaluate the empirical evidence before pharmacogenetic prescriptions can be made regarding naltrexone for alcoholism. As highlighted by Gelernter and colleagues (2007), attention to additional opioid genes, such
