Retina is part of the central nervous system responsible for perceiving light. The pigment epithelium (RPE) plays a crucial protective role by absorbing excess light, thereby reducing photooxidative stress and preserving retinal integrity. The widespread adoption of artificial lighting has increased exposure to artificial light in homes, workplaces, and personal electronic devices. This excessive exposure may disrupt circadian regulation, promote oxidative stress, and accelerate retinal aging, potentially compromising the protective functions of the RPE. Vitiligo is an autoimmune disease causing loss of pigment in the skin and RPE; it involves the destruction of pigment-producing cells. Melanin may compromise these protective mechanisms, potentially increasing susceptibility to light-induced retinal injury. Although the etiology is multifactorial and is incompletely understood, mechanisms including oxidative stress, autoimmune process, neurogenic factors, cytotoxic metabolites, defects in melanocyte growth and survival, and genetic predisposition have been implicated in the onset and progression. In vitiligo, the potential consequences of systemic melanocyte loss on ocular tissues remain poorly understood. We examine the hypothesis that loss of ocular melanin may increase susceptibility to light-induced retinal damage, and we argue for greater awareness of these extracutaneous risks in both clinical care and for informing public health policies.