In summary, our study shows that: (1) the CAD-predisposing genetic variant rs17514846 abolishes a methylated CpG motif in the FURIN gene; (2) the rs17514846 C allele interacts with the transcription factor MeCP2, which is known to often function as a gene repressor by binding to methylated CpG sites; (3) treatment with a DNA methylation inhibitor increases FURIN expression; (4) MeCP2 attenuation increases FURIN expression; (5) MeCP2 attenuation increases monocyte migration and proliferation, whereas a FURIN inhibitor diminishes this effect. This evidence concerns the gene MECP2 and coronary artery disorder.