Moreover, EC dysfunction induced by cyclophosphamide is mediated by the reduction of nitric oxide (NO) synthesis and endothelial progenitor cell production.36 On the other hand, increased expression of endothelin-1, NF-κB, Platelet factor 4 (PF4), and monocyte adhesion, in turn, participate in vasoconstriction and subsequently lead to hypertension incident.37 The gene discussed is PF4; the disease is hypertensive disorder.