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. 2019 Sep 26;105(4):773–787. doi: 10.1016/j.ajhg.2019.09.001

Table 1.

Primary and Secondary eQTLs Colocalized at GWAS Loci

Primary Signals Secondary Signals
Trait GWAS Signals Associated with ≥1 Gene Colocalized GWAS Signals Colocalized Genes Genes (%) for Which the Trait Risk Allele Is Associated with Decreased Expression Colocalized GWAS Signals Colocalized Genes Genes (%) for Which the Trait Risk Allele Is Associated with Decreased Expression
BMI 310 85 116 60 (52%) 12 11 4 (36%)
All lipids 186 56 62 31 (50%) 7 7 3 (43%)
HDL 73 25 30 18 (60%) 3 3 2 (67%)
LDL 64 16 18 8 (44%) 1 1 0 (0%)
Triglycerides 42 18 19 11 (58%) 2 2 1 (50%)
Total cholesterol 47 13 13 6 (46%) 2 2 1 (50%)
WHRadjBMI 157 48 57 35 (61%) 9 9 5 (56%)
WHR 134 40 49 32 (65%) 6 6 3 (50%)
T2D 115 28 37 20 (54%) 7 8 4 (50%)
Cardiovascular disease 28 9 10 6 (60%)
Adiponectin 11 4 4 2 (50%)
Any trait 874 231 287 152 (53%) 31 31 15 (48%)

Colocalized eQTL (FDR < 1%; p < 9.63 × 10−6) among 2,843 GWAS signals (variants clumped by LD r2 > 0.8) associated with one or more of 93 cardiometabolic traits. Each GWAS variant may colocalize with an eQTL for more than one gene. GWAS signals reported for multiple traits are included in counts of colocalized eQTLs for each trait, so signals and genes are not unique by row. Percentages expressed as the number of genes for which the GWAS risk allele was associated with decreased expression among all colocalized genes for that trait. No secondary eQTL signals were found to be colocalized with GWAS loci for cardiovascular disease or adiponectin.