Silencing of H19 can inhibit proliferation and induce apoptosis of vascular smooth muscle cells by regulating the miR-148b/WNT/β-catenin pathway [26], whereas overexpression of H19 can promote proliferation and suppress apoptosis by regulating MAPK and NF-κB signaling pathway [23], implicating the important values of H19 in atherosclerosis and hypertension that are risk factors for the formation of IA [5–7]. This evidence concerns the gene NFKB1 and atherosclerosis.