Since the lung developmental stages of mice and extremely preterm infants are similar at birth [22], and the lung phenotype of hyperoxia exposed neonatal mice resembles human BPD-PH [23,24,25,26,27], we decided to use this model to test the hypothesis that endothelial AMPKα1 is necessary to decrease hyperoxia-induced experimental BPD-PH burden in neonatal mice. This evidence concerns the gene PRKAA1 and bronchopulmonary dysplasia.