note that while one such SNP might easily be missed, many such SNPs could not be missed, and alone, such a SNP would contribute a locus specific to λS of only 1.04, which amounts to only a tiny fraction of the sibling relative risk in schizophrenia. To assess whether our negative data are consistent with the hypothesis of common variants explaining most of the sibling relative risk, we also investigated the relationship between the number of causal SNPs that might exist in the genome, given that all are undetected with 20% probability in our study, under a simple assumption that that all SNP effect sizes are equal and again assuming r 2 = 0.8 and MAF = 0.2 for each SNP. We find that for 2, 10 and 100 SNPs the limits on allelic odds ratios are 1.50, 1.38 and 1.27 respectively, while the combined contribution to total λS based on these SNPs (assuming they act independently on risk) are 1.07, 1.22 and 2.85 respectively. Taking these arguments to their logical conclusion, our data are also consistent with the possibility that 274 SNPs each with an OR = 1.22, r 2 = 0.8 and MAF = 0.2 lie undetected in
