The pathophysiological role of REDD1 in retinopathy was first demonstrated in a model of retinopathy of prematurity using Redd1-deficient mice11, as evidenced by a reduction in retinal neovascularization and apoptosis without altering retinal levels of vascular endothelial growth factor (VEGF), which is a major risk factor for retinopathy133, compared with WT mice. This evidence concerns the gene VEGFA and retinal disorder.