than trying to interpret the results from individual CNVs. A limitation of this approach is that the enrichment of CNVs seen in case–control studies is modest;2 indeed, one large study has reported no overall excess of CNVs in cases at all.4 This implies that among sets of CNVs drawn from cases, only a small proportion can be expected to be true risk factors for the disorder. Nevertheless, gene-set enrichment studies have supported conclusions drawn from consideration of genes affected by individual CNVs in schizophrenia16 by observing enrichment in schizophrenia of genes involved in a range of brain functions, for example, those encoding products involved in nitric oxide signalling, synaptic long-term potentiation and glutamate receptor signalling,17 or genes in a broad category corresponding to the gene ontology (GO) category ‘synaptic transmission'.18 However, it has been noted that the early gene-set studies did not allow for important confounders, in particular the large size of genes implicated in brain function, and that the conclusions that can be drawn are consequently unclear.19
