In the broadest sense, disulfuram (Antabuse), which inhibits aldehyde dehydrogenase (responsible for conversion of acetaldehyde to acetate) and targets the action of ALDH2 might be considered a drug with pharmacogenetic underpinnings. Although non-Asians do not carry the protective variant of rs671, disulfuram approximates its effects by inducing aversive reactions upon alcohol intake. A more specific instance in which genotype modulates treatment response for alcoholism comes from well-replicated studies of the Asn40Asp variant (rs1799971) in OPRM1 which encodes the mu-opioid receptor, and moderates the effectiveness of naltrexone (NTX; a mu-opioid antagonist) treatment [108]. Recent findings show that Asp40 (G) allele carriers have more positive subjective responses [109] and increased mesolimbic dopamine release following alcohol challenge compared to those homozygous for the Asn40 allele [A] [110]. There is evidence that NTX is efficacious in reducing heavy drinking only in Asp40 carriers [111-113]. GABRA2 variants also have been found to moderate treatment outcomes. Specifically, rs279858 was associated with drinking in individuals assigned to different psychotherapeutic treatments [114]. Although in that study there were no appreciable differences across treatment type (12-step vs. cognitive behavioral
