We thank Galvis et al.1 for their comments regarding the possible role of ultraviolet (UV) exposure in the regulation of ocular growth. As we noted in our report,2 although much still is unknown, results from animal studies suggest that UV light is not critical for the regulation of ocular growth during experimentally induced changes in scleral growth rates, and more specifically, does not underlie the ability of bright light to retard the development of experimental myopia. As discussed in our study,2 and as noted by the authors, the protection provided by bright light against the development of deprivation myopia has been obtained using UV-free lighting systems in all animal models tested (chicks,2–5 tree shrews,6 and rhesus monkeys7). Normal emmetropization also is modifiable in chicks by alterations in light intensity, again using UV-free systems.8,9 Therefore, UV exposure does not underlie the ability of bright light to retard the development of deprivation-myopia, or the ability of bright light to maintain normal untreated eyes in a hyperopic state. However, we have not tested whether broadening the spectral output of our lighting system to include UV output can induce an even greater protective effect against the development of myopia. This seems unlikely, as the development of deprivation myopia can be abolished in rhesus monkeys (20,000 lux)7 and chicks (40,000 lux)1 by bright light alone; therefore, UV exposure seems unnecessary. Instead, our data suggest that the ability of light to retard the development of deprivation myopia is driven by intensity-dependent increases in retinal dopamine release,4 although the role of spectral composition, in the visible range, is an area of interest (for review see the study of Rucker10).