Additionally, many earlier studies focused on TGFβ activation in hyperoxia-induced BPD utilized chronic 85% hyperoxia such as P0-P14 or P0-P28, both of which result in inflammation and fibrosis (Alejandre-Alcázar et al., 2007; Mižíková et al., 2015; Witsch et al., 2014a; Witsch et al., 2014b; Kumarasamy et al., 2009). Here, TGFB1 is linked to bronchopulmonary dysplasia.