Under this assumption, the individual variations in the DAT1 gene sequence can directly affect its epigenetic potential, so that we might construe large inter-individual differences in brain's DAT level as phenotypic manifestations of the combinatorial interplay of the DAT1 haplotype and epigenetic marks that jointly regulate the DAT. Empirical evidence supports our hypothesis; thus, the study of the effect of developmental exposure to tobacco smoke clearly demonstrated the risks of developing ADHD and the severity of the disease depends on the DAT1 genotype [7]. The gene discussed is SLC6A3; the disease is attention deficit-hyperactivity disorder.