The positive expression rate of Ki67 and CD31 proteins displayed a notable increase in lung tissues of neonatal mice with hyperoxia-induced BPD after being treated with oe-GABI vector with a remarkable decline in alveolar chord length and cell apoptosis compared with those treated with oe-NC vector (p < 0.05). This evidence concerns the gene PECAM1 and bronchopulmonary dysplasia.