A more recent report showed an association between a reward-related impulsivity endophenotype in response to a psychological stressor and the DRD2 C957T polymorphism among healthy adults [61]. Although the findings of the in vitro and in vivo characterization of this SNP were controversial [62,63], a follow-up PET study indicated that the increased binding potential of the T-allele was more important than the slightly increased DRD2 density, making the DRD2 availability of the T-allele higher compared to the C-allele [64]. To date, only the reduced DRD2 density of the TaqI A1-allele carriers has been convincingly replicated [19-22]. However, the DRD2/ANKK1 TaqIA polymorphism is probably not directly involved in DRD2 gene expression. The TaqIA SNP (rs1800497) is in linkage with TaqIB SNP (rs1079597) and with C957T SNP (rs6277) within the DRD2 gene, and these SNPs have also been associated with altered DRD2 density [21,64]. In addition, the TaqIA SNP is in linkage with a couple of non-synonymous SNPs of the ANKK1 gene [65]. Interestingly, a neighboring non-synonymous SNP (rs273849, Arg490His) of the ANKK1 gene has been recently shown to alter NF-κB function,
