The mechanism of endothelial dysfunction in RA is incompletely understood, but reduced tetrahydrobiopterin (BH4) availability or stability19 and increased production of reactive oxygen species have been suggested.20 Under basal conditions, endothelial nitric oxide synthase (eNOS) is responsible for NO production, but during inflammation, inducible NOS is also expressed in arterial endothelial cells. Here, NOS3 is linked to rheumatoid arthritis.