VEGFA and retinopathy of prematurity: This mouse model closely mirrors the pathological phenotypes observed in human retinopathy of prematurity, where hyperoxia initially reduces VEGF levels, causing vaso-obliteration, and subsequent hypoxia triggers a compensatory upregulation of VEGF, resulting in pathological neovascularization characterized by the overgrowth of immature vasculature and the formation of extraretinal vascular tufts 46 (Figure 5A and Figure S6A).