The preceding studies provide oblique inferences about genetic influences on delay discounting, but a small number of molecular genetic association studies have directly investigated the role of specific polymorphisms on discounting2. For example, in a moderately-sized nonclinical sample of young adults (N = 166), discounting was examined in relation to two genetic variants, the DRD2/ANKK13 Taq IA single nucleotide polymorphism (SNP; rs1800497) and the variable number of tandem repeats polymorphism in exon 3 of the dopamine D4 receptor gene (DRD4 VNTR) (Eisenberg et al., 2007). In this case, possession of at least one DRD2/ANKK1 A1 allele was associated with significantly greater discounting and possession of both the A1 allele and the long form of DRD4 VNTR was interactively associated with substantially more impulsive discounting. In other words, there was no main effect of DRD4 VNTR genotype, but the A1 allele carriers who also had at least one long version of DRD4 VNTR exhibited disproportionately high levels of impulsive discounting compared to the other genotype combinations. In a separate study of a locus related to the dopamine D2 gene, nonclinical young
