Genome-wide association studies (GWAS) provide a powerful method for identifying disease susceptibility loci for common diseases, offering the promise of novel targets for therapeutic intervention that act on the root cause of disease [Risch and Merikangas, 1996]. Within the last few years, many GWAS have been conducted and produced findings that generally support the hypothesis that the heritable risk of several major complex human diseases is attributable in part by common, low-risk variants [Easton et al., 2007; The Wellcome Trust Case Control Consortium (WTCCC), 2007; Hunter et al., 2007; COGENT Study, 2008; Eeles et al., 2008; Zeggini et al., 2008; Amos et al., 2008]. A typical GWAS calls for the use of high-throughput platforms to genotype a very large number of single nucleotide polymorphism (SNP) markers located throughout the human genome, in a set of cases and controls. Statistical tools are applied that compare the frequencies of SNP alleles between diseased and non-diseased individuals in a study cohort. Typically, only a very small fraction of SNPs are plausibly related to disease risk. Odds ratios (ORs) may be reported, to display
