The literature examining genetic influences on adolescent behavior is comprised largely of candidate gene studies. The advantage of candidate gene studies is that they potentially capitalize on known or hypothesized information about the underlying biology of the disorder under study in order to advance our understanding of genetic contributions to the outcome. The “usual suspect” candidate genes in the alcohol literature include neurotransmitters, receptors and alcohol metabolizing genes. For instance, DRD4, a dopamine receptor gene, has been linked to both heavy (Laucht et al., 2007) and binge (Vaughn et al., 2009) adolescent drinking as well as conduct disorder (Mota et al., 2013). A mu-opioid receptor gene, OPRM1, has been implicated in both alcohol misuse (Miranda et al., 2010) and “antisocial drug dependence” (Corley et al., 2008). The nicotonic receptor family has also been implicated in antisocial behavior and drug use (CHRNA2, Corley et al., 2008) and adolescent binge drinking (CHRNA4, Coon et al., 2014). Candidate gene studies, however, have not yielded the discriminatory power many researchers predicted (Dick et al., 2015). The literature is riddled with false positive reports, stemming