Although genes are unquestionably important for understanding individual differences in externalizing behaviors, the specific genetic architecture is unknown. Despite some major strides in elaborating the genetic basis of psychiatric illnesses and complex behaviors with polygenic causes, determining which specific genes and variants are involved remains largely elusive (Geschwind & Flint, 2015). How can it be that most of the substantial heritable variation in externalizing phenotypes appears “missing” (Manolio et al., 2009)? Current scientific consensus is that behavioral and psychiatric phenotypes, including externalizing behaviors, are influenced by a very large number of genes, each of which explains perhaps less than 1% of the total variability in a particular phenotype (C. Chabris, Lee, Cesarini, Benjamin, & Laibson, 2015; C. F. Chabris et al., 2013). Moving forward, psychology must grapple with the implications of a “many genes of small effect” model of complex behaviors and psychiatric diseases, including the enormous sample sizes necessary for a robust genome-wide association study (e.g., Rietveld et al., 2013) and the improbability of a large effect size for any single genetic variant (Dick et al., 2015).
