Since TGFβ1 has been recognized to be an important mediator in epithelial cell death and transformation to alveolar myofibroblasts in BPD [3,22], we also evaluated the role of TGFβ1 in vitro and in developmentally-appropriate in vivo models in relation to hyperoxia and JNK pathway inhibition. Here, MAPK8 is linked to bronchopulmonary dysplasia.