In conclusion, several steps have yet to be undertaken to advance this line of research. Specifically, agreement on the definition of patient populations is greatly needed along with replication and consistency in the clinical laboratory and clinical treatment arenas. Controlled prospective clinical pharmacogenetic trials need to be conducted using such definitions. Rodent and nonhuman primate models that have the greatest face validity for alcohol dependence should also be used in pharmacogenetic exploration and translation. The application of recent molecular findings regarding DNA methylation and additional functional OPMR1 variants offers a novel avenue for elucidating the neuropsychiatric implication of genetic variation in this gene. Finally, understanding how opioid genes interact with other relevant genes (epistasis), and gene products, such as DA receptors and transporters, for example, is likely to be a fruitful area of exploration. The effect of population heterogeneity, regarding sex and ethnicity, might also be crucial in understanding the pharmacogenetic effects of OPRM1 and other genes. In conclusion, while much progress has been made to elucidate the molecular, behavioral, and clinical effects of the Asn40Asp SNP on alcoholism etiology
