As for determinants of disrupted iron homoeostasis in these patients, data are limited but, in a small comparative observational study undertaken by ourselves (published in abstract form), there were significant increases in an array of plasma markers including: soluble transferrin receptor, free heme, iron saturation of transferrin, IL-6 and hepcidin; clearly demonstrating elevated levels of these iron indices in ES cohorts as compared to iPAH patients and healthy controls (Mumby et al., 2016). The gene discussed is HAMP; the disease is idiopathic pulmonary arterial hypertension.