To date, the most common measured genetic design for conduct disorder has been to examine a single variant in a handful of “usual suspect” candidate genes that have a purported biological function, typically related to serotonin and dopaminergic pathways or the stress response. There are numerous examples of this approach for conduct disorder related outcomes, as recently reviewed in Veroude et al. (2015). Although this approach is popular, it is problematic for a few reasons. First, history has shown that researchers have not been very good at identifying plausible candidate genes that confer risk for behavioral outcomes, and very few well-replicated associations have emerged from these hypothesized genes of interest (Bosker et al., 2011; Collins et al., 2012). Exceptions to this include variants in the alcohol dehydrogenase (ADH) gene cluster and alcohol outcomes (Gelernter et al., 2013; Thomasson et al., 1991) and nicotinic receptor genes (CHRNA5-CHRNA3-CHRNB4) for smoking outcomes (Broms et al., 2012; Tobacco and Genetics Consortium, 2010). Unlike alcohol and smoking behaviors, where there are concrete biological links to metabolism of the substance that may predispose some individuals to
