Retinopathy of prematurity is a devastating disease that affects around 100,000 infants yearly. Supplemental oxygen is necessary to prevent mortality in prematurely born infants; however, many infants on supplemental oxygen develop ROP. Recent work from our group and many other groups has highlighted the systemic nature of the disease. We have demonstrated that the interorgan metabolic crosstalk is central in the early phase of retinal development. Supplemental oxygen (hyperoxia) adversely alters this interorgan crosstalk. The aim of my newly formed lab is to discover the mechanistic basis of hyperoxia-induced vascular changes at cellular and systems levels. We use metabolomics, mass spectrometry, stable isotopes resolved flux analysis, lentiviruses/AAVs-based gene modification, cell culture, organoids, and in vivo mouse models to understand the mechanistic underpinning of retinopathy of prematurity and proliferative vascular disorders. The long-term goal of my lab is to develop metabolic treatments to prevent ROP.