Since alveolar development is angiogenesis-driven (Thebaud and Abman, 2007) and pro-angiogenic treatment has therapeutic potential in (experimental) BPD (Thebaud et al., 2005; Balasubramaniam et al., 2006; de Visser et al., 2009, 2010), the beneficial effect on alveolar enlargement may be explained by BMP9/ALK1-dependent stimulation of angiogenesis, which is supported by a reduction in tumor growth in mice and patients by anti-angiogenic therapy with pharmacological blockers of ALK1 (Cunha et al., 2010; Cunha and Pietras, 2011). Here, GDF2 is linked to bronchopulmonary dysplasia.