Genome-wide association studies (GWAS) in coronary artery disease (CAD) had identified 66 loci at'genome-wide significance'(P< 5× 10− 8) at the time of this analysis, but a much larger number of putative loci at a false discovery rate (FDR) of 5%(refs. 1, 2, 3, 4). Here we leverage an interim release of UK Biobank (UKBB) data to evaluate the validity of the FDR approach. We tested a CAD phenotype inclusive of angina (SOFT; n cases= 10,801) as well as a stricter definition without angina (HARD; n cases= 6,482) and selected cases with the former phenotype to conduct a meta-analysis using the two most recent CAD GWAS 2, 3. This approach identified 13 new loci at genome-wide significance, 12 of which were on our previous list of loci meeting the 5% FDR threshold 2, thus providing strong support that the remaining loci identified by FDR represent genuine signals. The 304 independent variants associated at 5% FDR in this study explain 21.2% of CAD heritability and identify 243 loci that implicate pathways in blood vessel morphogenesis as well as lipid metabolism, nitric oxide signaling and inflammation.