With respect to the identity of specific genes, there are important caveats that have to be borne in mind. First the strong statistical evidence in this study is for an excess representation of genes rather than for any individual gene per se. Second, association formally implicates regions, not genes, and in some cases, a single ‘true’ signal may, by LD, result in multiple genes being implicated. However, given the ratio of observed associated genes surpassing the thresholds to those expected, many of those doing so and reported in Supplementary Tables S1 and S2 are likely to represent true associations. A third caveat concerns the joint liability between schizophrenia and bipolar disorder. Our simulation procedures explicitly allow for the use of the same set of controls in the schizophrenia and bipolar GWAS analyses, and therefore our conclusion regarding an excess number of genes showing evidence for association across the two datasets is valid. However, the impact of using shared controls on the association evidence for any specific gene cannot be assessed by those procedures. Additional caution is therefore required with respect to the identities of the specific genes that appear to operate across both disorders (table S3).
