In our previous studies, we have also shown that the deletion mutations at the position reduce p50 expression and its transcriptional function of the NF-κB signaling pathway, down- and up-regulate the mRNA expression level of endothelial-type nitric oxide synthase, and inflammatory cytokine IL-6 genes, respectively, leading to endothelial cell dysfunction, apoptosis, and injury, thereby increasing the susceptibility to coronary heart disease [17]. The gene discussed is IL6; the disease is coronary artery disorder.