entirely consistent with the presented results and are available upon request. Third, the case–control design of this study does not allow conclusions regarding risks of nicotine dependence in the population as a whole but limits the interpretation of results to the transition to dependent smoking among those exposed to cigarette smoking. Fourth, this study’s statistical power to detect an effect the size observed for the H.S. peer smoking by rs16969968 interaction is low (61% at the multiple testing corrected 2-sided p-value of 0.0125 [36]). As low power increases the risk of false negative tests, the study’s failure to identify other statistical interactions must be considered tentative. Low statistical power does not, however, compromise our primary finding of the H.S. peer smoking by rs16969968 interaction. Fifth, these results require replication in an independent sample. Although the current study does not have a replication sample, it does meet other criteria suggestive of a credible finding [35]: 1) evidence-based selection of genes and environmental risk with main effects on the phenotype; 2) the GxE interaction was found with a functional SNP; and 3) significant results after correcting for multiple testing. Thus the interaction between rs16969968 and H.S. peer smoking is worth follow-up by
