statistically significant. However, it is unlikely that the SNPs themselves are causative, because the ~2.5 million SNPs in the HapMap 2 panel of Utah residents of Northern and Western European ancestry (CEU)26 represent only a fraction of all the polymorphisms segregating in the human population27. Assuming that multiple associated SNPs at a particular locus are not causative, it is unlikely that they are in LD with a single rare causal variant, especially for SNPs with minor allele frequency (MAF > 0.1), and it is also implausible that they are in LD with a single common causal variant (Supplementary Note). Therefore, it seems likely that there are multiple causal variants segregating at the same locus; however, this inference is indirect and inconclusive. With whole-genome sequence data, the conditional and joint analysis approach we present here will be helpful in identifying causal variants.
