A key framework for understanding the joint contribution of genetic and environmental influences on child outcomes is the gene–environment interaction (G × E), whereby exposure to a given environmental risk factor moderates the importance of genetic and/or environmental contributions to a given outcome (Plomin et al. 1977; Rutter et al. 2006). This etiological moderation can take many forms (Pennington et al. 2009; Burt, 2011). The most widely accepted of these represents a specific instantiation of the more general diathesis–stress model, in which genetic risk for a given behavior or outcome is expressed more fully in response to an environmental pathogen (Moffitt et al. 2006; Rutter et al. 2006; Gottlieb, 2007).
