Specifically, under oxidative stress, ROS produced in melanocytes could induce autophagy and activate the Nrf2 antioxidant pathway, remove toxic molecules, and maintain the redox homeostasis of melanocytes, while persistent stimulation of ROS might eventually lead to inactivation of autophagy and excessive activation of Nrf2 antioxidant pathway, breaking the redox homeostasis of melanocytes, resulting in premature senescence, decreased proliferation, and pigment synthesis, which may be involved in the onset of vitiligo. This evidence concerns the gene NFE2L2 and vitiligo.