by genome-wide significant SNPs on a chromosome is also proportional to its length, consistent with the conclusion made by Yang et al.5 using all SNPs (Supplementary Fig. 9). Our new results show that ~21%, ~24% and ~29% of phenotypic variance in independent validation samples is captured by the best ~2,000, ~3,700 and ~9,500 SNPs respectively selected in the discovery samples (Table 1), and that the correlation between actual and predicted height in independent samples from the same population has increased to 0.41 (maximum prediction R2 = 0.412 = 0.17, Fig. 2d). The results are consistent with a genetic architecture for human height that is characterized by a very large but finite number (thousands) of causal variants, located throughout the genome but clustered in both a biological and genomic manner. Such a genetic architecture may be described as pseudo-infinitesimal, and may characterize many other polygenic traits and diseases. There is also strong evidence of multiple alleles at the same locus segregating in the population and for associated loci to overlap with Mendelian forms, suggesting a large but finite genomic mutational target for height, and effect sizes ranging from minute (<1mm; ~0.01 SDs) to gigantic (>300mm; >3 SDs, in the case of
