Meta-analysis of genome-wide association studies (GWAS) involving tens of thousands of subjects have provided a wealth of new information on the genetic basis of coronary artery disease (CAD), yet common susceptibil-ity variants with achieved genome-wide significance explain only a small fraction of the heritability of CAD (≈10.6%).1,2 It has been proposed that much of the residual genetic risk may be attributable to rare variants with large effect.3,4 However, recent simulation, exome sequencing, and fine mapping stud-ies of established GWAS loci support the hypothesis that joint contributions from common variants with modest effects are likely to account for a sizeable fraction of the missing herita-bility of complex diseases.5–7 It is likely that many more common variants are linked to CAD but have not achieved genome-wide significance in GWAS because of small effect size or lower allele frequenc

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