The International Schizophrenia Consortium (ISC) reported evidence for a polygenic contribution to schizophrenia4. An independent family based study confirmed these results, greatly minimizing the possibility of population stratification artifact12. We reevaluated the polygenic model, dividing stage 1 samples into independent training and testing sets (Supplementary Note). The training set had 15,429 subjects (over twice the size of the ISC training set), and the testing set consisted of 6,428 individuals independent of the ISC report. The proportion of variance (Nagelkerke’s r2) explained in the testing set increased from 3% in the ISC to around 6% here (Supplementary Table 9 and Supplementary Fig. 6). This estimate is much lower than the true total variation in liability that is tagged by all SNPs because SNP effects are estimated with error3,4,22–25. The polygenic model appears to explain a substantial fraction of the heritability of schizophrenia4, as has been shown for other complex traits3,26–28. Some of these additional risk loci are likely contained near the most highly significant results of our stage 1 analysis. Supporting this hypothesis, of the top loci that did not reach
