Small animal models consistently demonstrate that inflammation is implicated in the pathophysiology of hypertension- and age-related vascular dysfunction [26,27] and there are overlaps between the structural and functional consequences of these pathologies and anthracycline-associated arterial toxicity, including extracellular matrix remodeling, degradation of elastin, and formation of advanced glycated end products [3,4,26,27]. The gene discussed is ELN; the disease is hypertensive disorder.