To establish a relationship between DNA damage, loss of BMPR2, and persistent PAH, we used transgenic mice in which Bmpr2 was deleted selectively in EC (EC-Bmpr2-/-) (Supplementary Fig. 1d–f), previously shown to have persistent pulmonary hypertension during reoxygenation after hypoxia18. This evidence concerns the gene BMPR2 and pulmonary arterial hypertension.