Third, our power to detect additive genetic effects and genetic correlations was limited. Neither genetic or environmental covariances nor any phenotypic correlations remained significant after correction for multiple testing. Nevertheless, the identification of genes that are both associated with nicotine dependence and found gene expression studies using human brains for these specific regions represents some validation. Similarly, the detection of significant environmental covariances in regions related to pleasure-related features of nicotine dependence also suggests the validity of the results. In conclusion, these results provide important preliminary evidence for specific biological pathways of brain structure to better understand the etiology of smoking-related behaviors.
