Replicability rates are high within Europeans, with 155 successful out of 181 attempts (85.6%), when only 9 positive replications (∼5%) would be expected under the null hypothesis of no association (binomial test, P<10−16). This excess was robust to the significance threshold (e.g. 122 observed vs. 0.18 expected if only replication attempts achieving P<0.001 are considered successful and 56 observed vs. 1.8×10−5 expected for a threshold of P<10−7, Table S5). Moreover, replicability rates within Europeans approach 100% when accounting for statistical power. For the 168 attempts for which we could calculate the power to replicate the original finding (Table S5), we observed 147 positive replications, which is almost identical to the expectation of 149.1 positive replications given that average power is 89.1% (see Materials and Methods). This is expected, since most GWAS already contain an internal replication phase [1], [24]. Interestingly, all diseases presented similarly high replicability patterns, with no traces of heterogeneity in replicability (Table S6). These results were consistent with previous partial reports of replication for individual diseases [17], [19] and confirmed that the subset of 190 genome-wide significant SNPs map in loci truly associated with disease in peoples of European ancestry.
