It is well documented that naltrexone is efficacious in the treatment of alcohol dependence (Anton et al., 2008; Kranzler and Van Kirk, 2001; Streeton and Whelan, 2001) and has been approved by the FDA for this indication since 1994. Nevertheless, the effect is moderate at best and it is recognized that not all individuals with an alcohol use disorder respond to it. Genetic differences have been suggested as one factor that might influence both response to alcohol and the ability of naltrexone to modify this response. There have been a number of animal and human clinical lab studies (Ray et al., 2011) suggesting that a single nucleotide polymorphism (SNP) in the mu opioid gene (A118G)1 leading to a missense asparagine to aspartate amino acid substitution at position 40 (asn40asp) (rs17799971) can lead to differences in alcohol effects and response to naltrexone. It has been shown that some of this enhanced alcohol response and drinking behavior in rodents engineered to have a homologous SNP is due to increased dopamine release in the nucleus accumbens (Ramchandani et al., 2011) which in general
