The findings of this exploratory study must be weighed with regard to the strengths and limitations of the study. First, population stratification was a possibility as participants were not exclusively from a homogenous ethnic background. To that end, controlling for population stratification by screening out non-White participants reduced the significance of the OPRK1^2 × medication interaction to a trend-level relationship. Thus, larger sample sizes affording greater statistical power are needed to confirm and extend these initial findings. Second, all participants received alcohol infusions only and there was no placebo (saline) infusion condition to control for alcohol expectancies. Third, in line with the purpose of the original study (Ray and Hutchison, 2007), participants were prospectively genotyped at the A118G variant of OPRM1. Thus, allele frequencies for OPRK1 and OPRD1 SNPs may not reflect those that would be observed if sampling from the population at random. However, as OPRM1 lies on chromosome 6, OPRK1 on chromosome 8, and OPRD1 on chromosome 1, it is unlikely that oversampling for 118G carriers biased the sample for the OPRK1 and OPRD1 markers. Next, given that
