Figure 1

The mechanisms that underlie observations of gene × environment interactions made in epidemiological studies (or gene × treatment interactions in clinical trials) likely involve a combination of epigenetic and transcriptional modifications. Although environmental exposures may be the primary triggers of these perturbations, the phenotypes themselves may also feed back to trigger both epigenetic and transcriptomic events, thus modulating the expression of disease phenotypes. The figure shows a simplification of how these processes might fit together. HDAC, histone deacetyltransferase; NCor, nuclear receptor corepressor; MeCP2, methyl CpG binding protein 2.