This decrease is attributed to enzyme shedding mediated by TNF-alpha-converting enzyme (TACE/ADAM17).8 However, prior hypoxia exposure eliminated this hyperoxia-induced decrease in ACE-2 in fetal lung fibroblasts.2 In models of BPD, hyperoxia has been suggested to increase ubiquitination and proteasome degradation of some proteins.13,14 ACE-2 ubiquitination has been shown to be involved in pulmonary hypertension and neurogenic hypertension.15,16. This evidence concerns the gene ACE2 and pulmonary arterial hypertension.