We draw four important conclusions from these results. First, from direct queries of the genome, we quantify the lower limit of the genetic contribution to schizophrenia; approximately one quarter of the variance in liability is directly tagged by common variants represented across the current generation of GWA arrays8 (Table 1) and this variance is shared between the sexes (Table 2). Second, we provide evidence that causal risk variants must include common variants (Figure 1d). Third, we provide evidence that the variance explained by chromosomes is linearly related to the length of the chromosome (Figure 1b), consistent with a highly polygenic model (many risk loci). Fourth, we find that the CNS+ gene set explains significantly (p = 7.6 × 10−8) more variation relative to the proportion of the genome it represents. Together our results provide guidance for the future of genetic studies in schizophrenia. Some have argued6,7,18 that common variants play little role in the etiology of schizophrenia and that the GWA approach for schizophrenia has been misconceived. Our results refute this conjecture that common variants play little role in the
