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Vitiligo is an autoimmune disease in which CD8+ T-cells target and destroy melanocytes, leaving areas of skin without pigment production. Nonsegmental vitiligo, the classical form of the disease, results in symmetrical, bilateral white patches. Vitiligo is a chronic, unpredictable disease, characterized by flares, with depigmentation and periods of disease arrest alternating. This process can be stressful and negatively impact one’s quality of life. Various hypotheses have been offered, including cellular stress causing degeneration of melanocytes, chemical toxicity causing melanocyte death, and neural changes that influence melanocytes or their ability to produce melanin. Recently, the interaction between oxidative stress and autoimmune-mediated melanocyte loss has been proposed as the primary pathogenesis of vitiligo. It is now well accepted that interferon-γ and/or C-X-C motif chemokine ligand 10 axis is functionally required for both progression and maintenance of vitiligo, making this pathway a potential therapeutic target. Most therapeutic interventions in the management of vitiligo have been developed based on this immunopathogenesis. This article aims to review the current understanding of the vitiligo pathogenesis.