Recent studies have shown that arterial stretch caused by the physicochemical factors of hypertension can promote the phosphorylation of ERK1/2/P38/JNK MAPK in VSMCs to increase their proliferation, migration, and apoptosis as well as promote arteriosclerosis [30], and cortistatin showed the potential in antiproliferation and antimigration effects in vascular smooth muscle cells stimulated by Ang II through suppressing ERK1/2/p38 MAPK/JNK signaling pathways [31]. The gene discussed is MAPK1; the disease is hypertensive disorder.