In addition to this modest increase in the number of discoveries, testing almost all common variants allows identification of many additional candidate variants that might underlie each association. For example, we find that rs11078928, a variant in a splice site for GSDMB, is in strong LD with SNPs near ORDML3 previously associated with asthma, Crohn's Disease, Type 1 Diabetes and rheumatoid arthritis, thus suggesting the hypothesis that GSDMB could be the causative gene in these associations. Although rs11078928 is not newly discovered, it was not included in HapMap or on commercial SNP arrays, and thus could not have been identified as associated with these diseases prior to this project. Similarly, a recent study31 used project data to show that coding variants in APOL1 likely underlie a major risk for kidney disease in African Americans previously attributed (at a lower effect size) to MYH9. These examples demonstrate the value of having much more complete information on LD, the almost complete set of variants in the regions, and putative functional variants in known association intervals.
