These exciting successes are expected to ultimately lead to improved understanding of underlying biological mechanisms; this knowledge can then translate to prevention and treatment efforts. However, once an initial disease association study has been completed, any SNP significantly associated with the phenotype in fact represents a finding for all genetic variants correlated with that original SNP through linkage disequilibrium (LD), as measured by r2. Even after a successful replication study, a set of correlated SNPs is expected to replicate. Therefore, multiple variants become candidates for functional and biological follow-up of that signal. There is a need for approaches that can help direct laboratory follow-up efforts to the most promising and potentially causal variants.
