Studies have shown that under the stress imposed by AMI (40), proinflammatory factors bind to TNF receptors on the cell membrane and activate the specific phosphorylation of the serine residue of κB, resulting in the activation of NF-κB, its entry into the nucleus; in the nucleus, NF-κB acts on gene promoters to accelerate the pathological process of atherosclerosis by advancing an inflammatory response, damaging the vascular endothelium, promoting the proliferation and migration of VSMCs and promoting vascular cell apoptosis (41). Here, NFKB1 is linked to atherosclerosis.