Definition: Evolving chalk white macules resulting from gradual destruction of melanocytes. Pathogenesis: 1. Self destruction of melanocytes: It is due to toxic intermediaries in the biosynthesis of melanin. 2. Neurogenic: Neurochemical substances like acetylcholine, epinephrine or non-epinephrine liberated at peripheral nerve endings destroy melanocytes. 3. Autoimmune (immunologic hypothesis): Association of vitiligo with alopecia, thyroiditis, diabetes mellitus, halo nevus, Addison’s disease, etc. suggests autoimmune process. Classification: (A) Localized: (i) Focal. (ii) Segmental. (B) Generalized: (i) Widespread: (a) Small macule. (b) Large macule. (c) Lip tip type. (ii) Universal. (C) Mixed: Widespread and segmental. Treatment: 1. Reassurance. 2. Photoprotection. 3. Camouflaging of the lesions with coloring agents. 4. Repigmentation attempt by: (a) Oral psoralen + UVA 320 to 400 nm/sunlight between 10 to 2 PM. (b) Local: Psoralen lotion, corticosteroid cream. 5. Skin k grafting of non-progressive lesions—suitable for surgery. Mechanisms of action of psoralen: 1. Photo conjugation, 2. Increase tyrosinase, 3. Increase number of functional melanocytes. 4. By promoting hypertrophy of melanocytes.