To dissect the functional contribution of FGFR1 in hyperoxia-induced BPD, we generated the genetically modified mouse in which Fgfr1 was conditionally deleted specifically in ECs (Fgfr1iΔEC/iΔEC) by crossing Fgfr1fl/fl mice with VE-Cadherin-(PAC)-CreERT2 mice (Figure 4A). Here, CDH5 is linked to bronchopulmonary dysplasia.