likely that many of these differences are due to multiple underlying rare variants that create different synthetic effects in the populations. There are also likely to be other diagnostics of synthetic associations observable in GWAS data. For example, one would expect distinctive extended haplotypes to be enriched in cases relative to controls in large regions surrounding GWAS signals that are synthetic (K. Wang, S. P. Dickson, C. A. Stolle, I. D. Krantz, D. B. Goldstein et al., unpublished data). Perhaps most importantly, the observation that association statistics are stronger for the causal sites in the vast majority of cases implies that in many cases, it should be possible to identify candidate causal sites using whole-genome sequence data surrounding GWAS signals and evaluate these for association. When the association is synthetic, association statistics would be expected to strengthen considerably when the correct causal sites are assayed.
