The outcome showed that the migration of VSMCs from the media to intima and their proliferation under the synthetic condition are responsible for arterial stiffness and arteriosclerosis; in addition to this, soluble DPP4 was proved to enhance cultured VSMC proliferation, and anagliptin was shown to downregulate the proliferation through restraining ERK phosphorylation (21); DPP4 significantly activates the MAPK and NF-κB signaling pathway, leading to the induction of inflammation and proliferation of VSMCs in vitro (73). This evidence concerns the gene DPP4 and arteriosclerosis disorder.