In spite of these shortfalls, we would suggest that these studies offer avenues for further research into the mechanisms of PASMC proliferation in PAH, and potentially in other wider aspects of vascular dysfunction, where disrupted iron homeostasis linked to the hepcidin/ferroportin axis that is responsible for either iron accumulation or iron deficits may be of importance. This evidence concerns the gene SLC40A1 and pulmonary arterial hypertension.