ancestry-informative markers (AIMs) and height, and did not detect a significant inflation of the test statistic for these AIMs (Supplementary Fig. 3; P = 0.219). All these results suggest that our estimate of variance explained by all SNPs is unlikely to be biased by population stratification. A subtle form of stratification in GWASs might occur because subjects are distantly related. We excluded any subjects with a relationship to another subject > 0.025. If distant pedigree relationships were an important cause of the estimated relationships, then all chromosomes of a pair of subjects should reflect this relationship. We found no correlation between relatedness estimated from different chromosomes (Supplementary Table 2). Thus, the relationships we estimate from SNPs are driven by LD among the SNPs. It is the same LD that causes a SNP that is not a causal variant to show an association with a trait such as height. In other words, our estimate of the variance explained by the SNPs is based on the same phenomenon as the SNP associations reported from GWASs (LD between SNPs and causal variants). However, we accumulate the variance explained by all SNPs and so are not limited by the need for individual SNPs to
