Our previous studies demonstrated that the hypoxia-induced BPD originated from persistent ER(endoplasmic reticulum) stress, and finally led to upregulation of CHOP expression and cell death [3], Wagenaar et al observed that a missense mutation in cytoplasmic helix 8 of LPAR1(lysophosphatidic acid receptor 1) can protect the lung of neonatal rats against the hyperoxia-induced BPD, moreover, treatment of Ki16425 toward BPD experimental mode confirmed this result that blocking of LPAR1 may be a novel therapeutic option for BPD [4]. This evidence concerns the gene LPAR1 and bronchopulmonary dysplasia.