Recent data of our group demonstrated a marked endothelial dysfunction in PA characterized by an increase of reactive oxygen species and by an increased expression of p47phox [8] as well as a decreased BMPR2 lung expression together with exaggerated response of PA to 5-HT (authors unpublished observations) in rats treated with streptozotocin as an insulin-dependent diabetes model. This evidence concerns the gene NCF1 and endothelial dysfunction.