FGF-21 has been linked to ROP mainly through experimental studies using the mouse model of oxygen-induced retinopathy (phase I and II ROP) as well as the mouse model of hyperglycemia-associated retinopathy (phase I ROP). In mouse hyperglycemia-associated ROP, FGF-21 administration promoted physiological retinal vessel growth through mitochondrial lipid oxidation mediated by adiponectin. In preterm infants, low serum adiponectin levels, linked to insufficient DHA levels, have been identified as a risk factor for ROP. Here, FGF21 is linked to retinopathy of prematurity.