may in fact be a function of one or more gene × environment interactions, meaning that genetic influences may only be evident in individuals with certain environmental exposures, such as early life stress (e.g., Enoch, 2012). Alternatively, if level of impulsive discounting is indeed largely a function of low corticomesolimbic dopamine tone, it is possible that an array of combinations of genetic variants might contribute to this systems-level characteristic, making impulsive discounting nonspecific to individual loci and an emergent property of the system. For example, variants responsible for transporter molecules clearing dopamine from the synapse and variants responsible for differences in the density or binding potential of dopamine receptors subtypes could both lead to the same aggregate profile of dopaminergic activity, high or low. Based on the model in Figure 4, these systems-level effects would be associated with commensurate differences in discounting, but this would happen by way of entirely different loci. Capturing relationships like this may require novel strategies, such as examining aggregate genetic risk scores (e.g., Derringer et al., 2010; Karlson et al., 2010) or examining combinatorial genetic profiles that have known systemic effects (e.g., contrasting individuals who are positive and negative for a panel of risk or
