Single nucleotide polymorphisms (SNPs) in the opioid receptor genes (OPRM1, OPRD1, and OPRK1) are obvious candidates for involvement in liability for heroin dependence. OPRM1, which encodes the mu opioid receptor (MOR) at which heroin and other commonly used opioids exert their primary effects (e.g., analgesia, reward, and dependence), (Le Merrer et al. 2009) has understandably been the most highly investigated of these genes. 118 A >G (rs1799971) is an exonic OPRM1 SNP that results in an amino acid substitution (Bond et al. 1998) which reportedly reduces mRNA expression (Zhang et al. 2005) and alters stress responsivity (Wand et al. 2002). Initial excitement over reported association of this seemingly ideal candidate with heroin dependence [e.g., (Bart et al. 2004)] has been tempered by subsequent findings. Although meta-analyses (Glatt et al. 2007; Coller et al. 2009) have concluded that the preponderance of evidence does not support a significant role in opioid dependence liability for this SNP, its potential involvement in the pathophysiology of other addictive disorders continues to be actively investigated (Ray et al. 2011). Overall, no associations involving OPRM1 SNPs have
