The decrease in VWF expression promotes the proliferation and migration of endothelial cells, which is related to re‐endothelialization.[47] In addition, upregulation of NFE2L2 in drug condition plays a role in cellular protection against oxidative stress and alleviates the transition of VSMC phenotype.[47, 99] NFKB1, VCAM1, and PTGS2, which were upregulated in IH condition and diminished in drug condition, are related to vascular inflammation and arterial diseases.[47, 102, 103] BMP2, which showed increased expression in the IH and drug conditions, is an osteogenesis marker of VSMCs.[48]. The gene discussed is VCAM1; the disease is inflammation.