Our results have several implications. First, they outline a role for multiple genes and biological pathways that were previously not known to regulate height, substantiating the ability of unbiased genetic approaches to yield new biological insights. The identification of these genes not only expands our knowledge of human growth but also promotes these genes as candidates for as yet unexplained syndromes of severe tall or short stature. Second, these findings convincingly confirm the polygenic nature of height, a classic complex trait, and demonstrate that, at least for this trait, increasingly large GWA studies can uncover increasing numbers of associated loci. Third, each variant makes only a small contribution to phenotypic variation (although determining the total contribution of each of the loci reported here requires much more comprehensive resequencing and genotyping); thus, either many hundreds of common variants influence complex traits such as height and/or other genetic contributors (for example, gene-gene or gene-environment interactions, rare variants with large effects, or uncaptured genomic features such as structural polymorphisms) will play a significant role. In particular, because the quality-control criteria used in the
