Most ongoing genome-wide association studies (GWAS) rely on a commercial SNP genotyping panel that directly assays only a small fraction of SNPs in the human genome [Carlson et al., 2003; The International HapMap Consortium 2005]. In these scans, the majority of SNPs in the genome must be evaluated indirectly using one or more of the genotyped SNPs as proxies [Barrett and Cardon, 2006; Pe’er et al., 2006]. Despite the ability of individual genome-wide association scans to identify common alleles that make large contributions to disease risk and a subset of the loci with smaller effect [Hirschhorn and Daly, 2005], many alleles that contribute to complex disease can only be identified through the meta-analysis of multiple genome-wide scans [for specific examples, see Lettre et al., 2008; Sanna et al., 2008; Willer et al., 2008, 2009]. Although it is possible to assign SNPs genotyped in each study as proxies for SNPs genotyped in the other studies [Carlson et al., 2004; de Bakker et al., 2005; Lin et al., 2004; Nicolae, 2006; Zaitlen et al., 2007], meta-analyses of GWAS conducted in this manner
