Fernandez-Gonzalez et al. [19] reported that HO-1 overexpression improved pulmonary inflammation, arterial remodeling, and right ventricular hypertrophy in a murine model of hyperoxia-induced BPD, but it did not prevent alveolar simplification, which is one of the characteristic pathological findings of BPD [20]. This evidence concerns the gene HMOX1 and bronchopulmonary dysplasia.