The emerging research on the OPRM1 gene in alcoholism has been fueled by its translational potential, particularly naltrexone pharmacogenetics (Heilig et al., 2011; Heilig et al., 2010). Some clinical studies have shown that G-allele carriers may respond better to naltrexone (Anton et al., 2008; Oslin et al., 2003), while other studies have failed to replicate these findings (Gelernter et al., 2007). Laboratory studies have shown that G-allele carriers may experience greater blunting of alcohol reward on naltrexone (Ray and Hutchison, 2007; Setiawan et al., 2011), which in turn may explain its differential clinical efficacy in some trials. These pharmacogenetic effects have also been shown in non-human primates (Barr et al., 2011). While the clinical utility and mechanisms underlying the OPRM1 × Naltrexone interaction is not fully established(Ray et al., 2012), it is critical to extend the human laboratory findings from heavy/social drinking samples to individuals with alcohol dependence.
