more explicitly than the field was often ready to accept, the tradeoff between false positive and false negative rates in the criteria used to identify genes as being “positive” in any particular analysis (for a detailed consideration of this issue see (Sebastiani, Timofeev, Dworkis, Perls, & Steinberg, 2009)). Several aspects of the approach used in this series of studies mitigated concerns about false positives, including the identification of not just single SNP associations, but clusters of positive SNPs in specific genes (Q. R. Liu, et al., 2006). Furthermore, the initial strategy of identifying positive findings in both European-American and African-American subjects was extended to other drug dependent populations (Johnson, et al., 2006). Additionally, the original two populations, although not necessarily the same subjects, were assessed in a series of studies using increasing marker densities. Thus, it is important to consider the findings as a whole, and the degree of replication across those studies, and other studies that have been completed subsequently. As discussed in Drgon et al. (2011), the definition of “replication” in GWAS for major gene effects that involve the same allele is relatively straightforward, but this is not the circumstance for phenotypes that have a polygenic genetic architecture,
