Considering that both β1 and β2-ARs are expressed in the retina [37–40], that hypoxia increases VEGF levels presumably through overactivation of the β-adrenergic system as suggested by norepinephrine accumulation in response to hypoxia [41, 42], that β-AR blockade is effective in mouse models of retinal neovascular diseases, our assumption was that the use of β-AR blockers, such as propranolol, could be useful for the treatment of ROP in infants. The gene discussed is ADRB2; the disease is retinopathy of prematurity.