Although large sample sizes are needed to pinpoint the variants responsible for the heritability of height (and larger samples in multiple ancestries will probably be required to map these at finer scale), the prioritization of relevant genes and gene sets is feasible at smaller sample sizes than that required to account for the common variant heritability. Thus, the sample sizes required for saturation of GWAS are smaller for identifying enriched gene sets, with the identification of genes implicated as potentially causal and mapping of genomic regions containing associated variants requiring successively larger sample sizes. Furthermore, unlike prediction accuracy, prioritization of genes that are likely to be causal and even mapping of associated regions is consistent across ancestries, reflecting the expected similarity in the biological architecture of human height across populations. Recent studies using UKB data predicted that GWAS sample sizes of just over 3 million individuals are required to identify 6,000–7,000 GWS SNPs explaining more than 90% of the SNP-based heritability of height52. We showed empirically that these predictions are downwardly biased given that around 10,000 independent associations are, in