Moreover, Sun et al. showed that increased levels of NDUFA4L2 are crucial in advancing hypoxia-induced pulmonary hypertension by promoting ROS production and pulmonary arterial smooth muscle cell (PASMC) proliferation, suggesting that targeting NDUFA4L2 could be a promising novel therapeutic approach for PAH16. Here, COXFA4L2 is linked to pulmonary arterial hypertension.