To that end, the A118G single nucleotide polymorphism (SNP) of the mu-opioid receptor gene (OPRM1), has garnered much interest as a potential moderator of SR.[17] Numerous laboratory studies have demonstrated that G-allele carriers experience the stimulating, hedonic effects of alcohol more strongly than A homozygotes.[18] However, a study of non-treatment seeking participants with alcohol dependence found that A homozygotes experienced more stimulation than G carriers, and a study of heavy drinkers reported no differences in SR between OPRM1 genotype. These mixed findings may stem from differences in alcohol use severity among samples, as the allostatic model of addiction contends that individuals shift from reward to relief drinking as alcohol use disorder progresses.[19] Thus, it is possible that social drinkers and individuals with mild alcohol use disorder may experience the hedonic effects of alcohol as most salient while individuals with more severe alcohol use disorder may consume alcohol for its negative reinforcing properties (i.e., to reduce withdrawal symptoms). The use of retrospective, instead of real time, self-reports of SR as well as differences in ethnicities of samples may further contribute to discrepancies in studies exploring the effects of the OPRM1 gene and SR.