By compiling data from 299 GWAS for 28 different diseases, we build a large database of discovery-and-replication patterns of SNPs associated with complex disease. We evaluate the extent to which risk variants discovered in Europeans replicate in posterior studies performed on individuals of European, East Asian and African ancestries and compare the risk effect sizes found across populations. We also examine the extent up to which statistical power and differences in Linkage Disequilibrium among populations explain replication failures. Our results describe the patterns of replicability of GWAS across disease, evaluate how transportable these results are across populations and allow for inferences about the relative roles of rare and common variants in explaining current GWAS results.
