The main roles of hyperphosphatemia in vascular calcification include: inducing the transition of VSMCs from contractile to osteochondral phenotype and mineralization of the extracellular matrix of VSMCs, inducing apoptosis of VSMCs, inhibiting the differentiation of monocytes or macrophages to osteoclast-like cells, increasing fibroblast growth factor 23 (FGF23) levels, and decreasing Klotho expression [67]. The gene discussed is FGF23; the disease is hyperphosphatemia.