That we found significant excess of associated genes at most thresholds provides molecular genetic evidence that has been lacking for the existence of substantial numbers of detectable common alleles of small effect in each of the disorders we tested. Given an assumption of relatively low power to detect genes (which is difficult to estimate given the variation in numbers of SNPs/gene and the number of independent signals/gene, each of different effect size and allele frequency) the excess of associated genes we have observed is likely a small proportion of the total. These data therefore support an important polygenic contribution to liability to both schizophrenia and bipolar disorder. Such a contribution to schizophrenia has previously been suggested by attempts to model the expected prevalence of the disorder among relatives of probands based upon various modes of transmission24,25. We also note our data are incompatible with the hypotheses recently advanced elsewhere that there is only a single schizophrenia risk gene or indeed that all risk is epigenetic26. The existence of multiple genes of small effect suggests that the collection and application of
