Recent breakthroughs in high throughput genotyping technologies have ushered in the era of genome-wide association studies (GWAS) that have reproducibly identified thousands of genetic variants associated to many diseases and complex traits [1]. GWAS leverage the linkage disequilibrium (LD) patterns among genetic markers for probing genetic variation beyond the typed variants. Thus, it is often the case that the associated variant is not itself biologically causal, but rather, a proxy as a result of LD. Identification of causal variants underlying risk loci is performed within fine-mapping studies [2], [3], [4] through sequencing (or array typing and imputation) followed by variant prioritization using marginal association statistics or posterior probabilities [5], [6], [7]. Using these measures, a set of top candidate variants is selected for testing in functional experiments to validate biological causality.
