A study has indicated that in preclinical PAD models, the increased expression of VEGF165b in macrophages inhibits the phosphorylation of VEGFR1, leading to an increase in downstream S100A9, and an increase in calcium influx, thereby inducing MI‐like polarization of macrophages, ultimately inhibiting angiogenesis and reperfusion recovery in ischemic muscles of PAD.125. The gene discussed is S100A9; the disease is peripheral arterial disease.