An increase in NOX activity contributes to the increased autophagy in persistent pulmonary hypertension (PPHN)–pulmonary artery endothelial cells (PAECs), whereas the increase of autophagy can reciprocally promote the formation of ROS through NOX-2, leading to impaired angiogenesis involving PPHN-PAECs (Teng et al., 2012). Here, CYBB is linked to persistent fetal circulation syndrome.