A major goal in mental health research is to identify endophenotypes that are neurobehavioral measures of psychiatric disorder liability. While complex in their application, endophenotypes are conceptually simple: in the causal chain between genes and clinical outcome, endophenotypes are a laboratory-based measure of a component of that chain that are causally closer to gene action than the eventual clinical outcome. Endophenotypes are usually defined as laboratory-based measures that are associated with a clinical outcome, heritable, manifest in an affected individual even when the disorder is not active, and cosegregate with the associated clinical outcome in families (Gottesman & Gould, 2003). We have also argued previously that to qualify as an endophenotype, v. a putative endophenotype, the laboratory-based measure should also show robust and reliable associations with genetic variants through genetic association studies (Iacono et al. 2016). Endophenotypes are also thought to be more genetically homogeneous than their associated clinical outcomes (Cannon & Keller, 2006), and so effects of individual genetic variants on endophenotypes are suspected to be larger and possibly easier to detect than the effect of those variants on
