The study finds that the non-risk allele (the C allele) is subjected to methylation of a CpG motif at the rs17514846 site, interacts with the transcription factor MeCP2 (that often acts as a gene repressor by binding to methylated CpG sites [23,24]), and results in reduced expression of FURIN, whereas the C to A change of this SNP in the CAD risk allele (the A allele) abolishes the CpG motif, diminishes MeCP2 binding, and leads to increased FURIN expression. Here, MECP2 is linked to coronary artery disorder.