A number of linkage and association studies searched for specific genes contributing to heritability of P3 amplitude and other ERP characteristics documented by twin studies. Hill et al. (1998) reported an association between a polymorphic marker for D2 dopamine receptor gene (DRD2 Taq I, later localized in ANKK1 gene) and P3 amplitude in children of alcoholics, with A1 allele carriers showing reduced P3 amplitude. Another study (Anokhin et al., 1999b) has replicated this association in a sample of adults, mostly from families with alcoholism. Furthermore, this study found a significant interaction effect of this genetic polymorphism and tobacco smoking status on P300, such that smokers with A1 allele showed the largest P3 amplitude reduction. One possible explanation for this finding is that A1 allele increases the riskfor nicotine addiction, but this association is moderated by P3, with reduced P300 amplitudes facilitating addiction in A1 carriers and high P3 amplitude acting as a protective factor. According to this hypothesis, P3 is a moderator, rather than mediator, of genetic risk (Anokhin et al., 1999a). This hypothesis is consistent with the notion that
