SNPs identified from reference data. Further analyses in additional samples are needed to identify the causal sequence that is the source of the signal detected at rs10482672. Third, it is uncertain whether results generalize to non-white populations. To the extent that the tagging SNPs we observed captured less variation in the surrounding sequence in African-American as compared to European-American children, it could lead to spurious null findings in the African-American sample. Moreover, we were unable to account for the likely substantial genetic diversity within the African-American sample. The lack of genome-wide data in our study precluded the use of a comprehensive strategy to address potential confounding by racial admixture. It is also the case that race differences could exist in base rates or reporting behaviors related to the outcomes we studied (Costanzo et al., 2007). However, previous Fast Track evaluations have found no evidence for race differences in program impacts on similar outcome measures (CPPRG, 2007; 2011; 2014). Fourth, analyses focused on a single gene, the glucocorticoid receptor NR3C1. We expect there are dozens, if not hundreds of genes and intergenic loci involved in regulating response to Fast Track and other complex behavioral interventions. Ultimately, genome-wide investigations of variants moderating
