Vitiligo is an acquired depigmentary disorder due to autoimmune destruction of melanocytes affecting the skin and/or mucous membranes and occasionally eyes, hair bulbs and ears, leading to alterations in both structure and function of these organs. It has polygenic inheritance and stress and trauma are potential triggers. The pathogenesis of vitiligo is complex but the intrinsic defect of melanocytes and autoimmune destruction of melanocytes are present in all cases. It has four conventional types: vitiligo vulgaris (most common), acrofacial, segmental, and universal. The classical presentation is asymptomatic, well-demarcated, chalky-white, round or oval macules with scalloped margins with or without leukotrichia. Histopathology reveals complete absence of melanocytes, increased numbers of Langerhans cells in epidermis and lymphocytic infiltrates and/or spongiotic foci at the edge of the active vitiligo lesions. A 11-year-old child presented to our outpatient department with slowly progressive asymptomatic nonscaly depigmented patches on face and white eyebrow hairs for past 2 years. Absence of pre-existing dermatosis or chemical application at the site, positive family history, morphology and negative KOH smear ruled out other close possibilities such as chemical leukoderma and pityriasis versicolor. Medical and surgical treatment of vitiligo includes topical/systemic steroids, immunomodulators, phototherapy, excimer laser and skin grafting surgeries.