Early efforts to localize and identify genes that contribute to risk of common chronic diseases often used either candidate gene studies or family-based linkage studies, which suffered from low statistical power, lack of replication, and low precision (1). Although there were successes, progress was generally slow. Recently, genome-wide association studies (GWAS) have proven to be productive when they have adequate sample sizes and replication opportunities. Their primary aim is to identify novel genetic loci associated with inter-individual variation in the levels of risk factors, the measure of subclinical disease, or the risk of clinical events. The method does not require assumptions about a priori biologic involvement, is precise in its ability to localize genetic effects to relatively small regions of the genome, and can be extended to evaluate potential gene-environment interactions.
