Previous studies have reported that LPS enters the systemic circulation and causes an inflammatory response involved in the development of cardiovascular events; thus, it can serve as a biomarker of CAD [38, 39]SMYA was found to lower the expression of LPS and inhibit TLR4/NF-κB signaling, reducing the expression of downstream inflammatory factors and circulating levels of inflammation. This evidence concerns the gene NFKB1 and coronary artery disorder.