Although the status of mitochondrial DNA damage in pulmonary arterial hypertension patients with or without BMPR2 mutations is currently unknown, it is plausible to speculate that the BMPR2–RAD51 axis may play a role in the maintenance of pulmonary vascular homeostasis by protecting the integrity of not only nuclear DNA but also mitochondrial DNA, since RAD51 functions both in the nucleus and in the mitochondria63. This evidence concerns the gene RAD51 and pulmonary arterial hypertension.