Furthermore, according to Arvunescu et al. alongside with other proinflammatory mediators such as tumour necrosis factor-α (TNF-α), interleukin-1, IL-6, fibrinogen, C-reactive protein and myeloperoxidase (MPO), iNOS activation also leads to inhibition of cardiac contractility and induction of oxidative stress through NO-related cytotoxicity, playing a major role in the pathophysiology of heart failure with preserved ejection fraction and ischaemic cardiomyopathy (55). The gene discussed is MPO; the disease is cardiomyopathy.