Abstract
Psychiatric disorders have a heterogeneous biological basis, where environmental factors interplay with non-mendelian genetics to produce complex cognitive/behavioural syndromes such as schizophrenia. Recent findings indicate a proportion of schizophrenia is associated with genomic copy number variation, suggesting that alteration of gene expression levels rather than direct mutation may play a role. Epigenetic mechanisms could be the crucial link between external stimuli and gene expression, influencing schizophrenia risk. These are dynamic reversible systems that offer much promise as targets for future therapies.