These findings indicated that the overexpression of TLR4 may be due to the reduction in HDAC1, DNMT1, and SUV39H1 recruitment by RFX1, which, in turn, led to an increase in histone acetylation and a decrease in DNA methylation and H3K9 trimethylation in the TLR4 promoter region in CAD patient CD14+ monocytes. Here, RFX1 is linked to coronary artery disorder.