Furthermore, in a mouse model of oxygen induced retinopathy, which is meant to mimic retinopathy of prematurity (ROP) in humans, which also results in an inability to vascularize the retinal periphery, activation of S1PR1 signaling or inhibition of S1PR2 signaling using genetic models in mice resulted in more normal retinal vascular patterning (34, 40). Here, S1PR1 is linked to retinopathy of prematurity.