Vitiligo is a common depigmentation disorder characterized by the loss of melanocytes, primarily due to immune-mediated mechanisms. The review discusses the pathogenesis of vitiligo, distinguishing between non-segmental and segmental forms. Non-segmental vitiligo involves immune-mediated destruction of melanocytes by cytotoxic T cells, while segmental vitiligo is associated with somatic mosaicism and localized immune responses. Both forms share similarities in inflammatory components and immune pathways, but segmental vitiligo is less associated with systemic autoimmune diseases and has a more localized presentation. The JAK-STAT pathway, particularly IFN-γ, plays a crucial role in melanocyte destruction, and JAK inhibitors are effective in treating vitiligo by inhibiting this pathway. However, long-term treatment is often required for optimal results. Topical treatments, including corticosteroids, calcineurin inhibitors, and JAK inhibitors, are commonly used, while systemic treatments such as JAK inhibitors and immunosuppressants are also effective. The review highlights the importance of balancing immune responses to prevent excessive melanocyte destruction and reduce cancer risk. Future treatment options focus on enhancing Treg function, targeting immune checkpoints, and developing localized therapies to minimize systemic side effects. The study also emphasizes the need for alternative melanocyte stimulants beyond UV light to improve repigmentation. Overall, the review underscores the complex interplay between immune mechanisms and melanocyte survival in vitiligo, highlighting the need for personalized and comprehensive treatment approaches.Vitiligo is a common depigmentation disorder characterized by the loss of melanocytes, primarily due to immune-mediated mechanisms. The review discusses the pathogenesis of vitiligo, distinguishing between non-segmental and segmental forms. Non-segmental vitiligo involves immune-mediated destruction of melanocytes by cytotoxic T cells, while segmental vitiligo is associated with somatic mosaicism and localized immune responses. Both forms share similarities in inflammatory components and immune pathways, but segmental vitiligo is less associated with systemic autoimmune diseases and has a more localized presentation. The JAK-STAT pathway, particularly IFN-γ, plays a crucial role in melanocyte destruction, and JAK inhibitors are effective in treating vitiligo by inhibiting this pathway. However, long-term treatment is often required for optimal results. Topical treatments, including corticosteroids, calcineurin inhibitors, and JAK inhibitors, are commonly used, while systemic treatments such as JAK inhibitors and immunosuppressants are also effective. The review highlights the importance of balancing immune responses to prevent excessive melanocyte destruction and reduce cancer risk. Future treatment options focus on enhancing Treg function, targeting immune checkpoints, and developing localized therapies to minimize systemic side effects. The study also emphasizes the need for alternative melanocyte stimulants beyond UV light to improve repigmentation. Overall, the review underscores the complex interplay between immune mechanisms and melanocyte survival in vitiligo, highlighting the need for personalized and comprehensive treatment approaches.