Our hypothesis is that also in human preterm newborns with ROP, VEGF overexpression could be induced by beta2-AR stimulation, and that propranolol, a well-tolerated, non-selective, beta-AR blocker, administered in preterm newborns when a precocious phase of ROP is detected, could reduce the progression of the disease. The gene discussed is VEGFA; the disease is retinopathy of prematurity.