Our secondary objectives were to use the data to identify a number of putative susceptibility genes and also to determine if there is overlap between schizophrenia and bipolar susceptibility. Taking the latter first, although the findings are less robust than the main results, at several thresholds, we observed an excess of associated genes common to schizophrenia and bipolar disorder. These findings support the specific hypothesis that some genes influence risk beyond traditional diagnostic boundaries. That only a small proportion of genes overlapped should not be taken as indicative that this provides an estimate of the extent of shared risk; the small effect sizes inevitably lead to low power for one sample to ‘replicate’ findings observed in the other. Similar considerations may explain why the excess in overlap was observed at the weaker thresholds of significance; any one gene detected in one study is unlikely to be replicated at similar levels of significance in another2,6. Much larger studies will be required to explore and characterize the extent of the overlap.
