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Genome-wide association studies have revealed an association between the genetic variant rs17514846 in the <i>FURIN</i> gene and coronary artery disease. We investigated the mechanism through which rs17514846 modulates <i>FURIN</i> expression. An analysis of isogenic monocytic cell lines showed that the cells of the rs17514846 A/A genotype expressed higher levels of <i>FURIN</i> than cells of the C/C genotype. Pyrosequencing showed that the cytosine (in a CpG motif) at the rs17514846 position on the C allele was methylated. Treatment with the DNA methylation inhibitor 5-aza-2′-deoxycytidine increased <i>FURIN</i> expression. An electrophoretic mobility super-shift assay with a probe corresponding to the DNA sequence at and around the rs17514846 position of the C allele detected DNA-protein complex bands that were altered by an anti-MeCP2 antibody. A chromatin immunoprecipitation assay with the anti-MeCP2 antibody showed an enrichment of the DNA sequence containing the rs17514846 site. siRNA-mediated knockdown of MeCP2 caused an increase in FURIN expression. Furthermore, MeCP2 knockdown increased monocyte migration and proliferation, and this effect was diminished by a FURIN inhibitor. The results of our study suggest that DNA methylation inhibits <i>FURIN</i> expression and that the coronary artery disease-predisposing variant rs17514846 modulates <i>FURIN</i> expression and monocyte migration via an allele-specific effect on DNA methylation.