Overall these studies suggest that a systemic increase in IGFBP-3, potentially achieved through improved nutrition, could prevent or slow the progression of BPD by increasing eNOS - mediated NO production in lung microvascular endothelial cells, by downregulating inflammation and reducing IFNγ and activation of IFNγ targets, while promoting IGF-1 beneficial effects (Figures 2, 3). This evidence concerns the gene IGF1 and bronchopulmonary dysplasia.