In psoriasis, tazarotene acts by modulating the three main pathogenic features: abnormal differentiation, hyperproliferation of keratinocytes, and inflammation. 3 As with other topical retinoids, adverse events with tazarotene are limited to local effects, most frequently being erythema, pruritus, burning/stinging and, rarely, pyogenic granuloma in patients with psoriasis. 4 However, retinoids are not known to cause depigmentation. Topical use of retinoic acid (RA) produces improvement in hyperpigmentation by reducing the number of functioning melanocytes and/or in inhibiting their ability to synthesize melanin. 5 Retinoids are potent inhibitors of mammalian GSTs (glutathione-s-transferase) and this makes cells more susceptible to the cytotoxic effects of chemicals. 6 We do not have the exact explanation for this observation besides the above-mentioned biochemical mechanisms or the local irritation and erythema following tazarotene causing depigmentation by Koebnerization. The occurrence of vitiligo within an area treated with tazarotene does not illustrate definite direct cause but probably does indicate the need for vigilance to see whether this association occurs again. Clinicians should be aware of potential pigmentary changes, particularly when using tazarotene on areas of skin that are readily visible or in patients of vitiligo for treatment of other dermatoses. We suggest that this rare but important observation should be considered as a potential side-effect of tazarotene. Mays S. The pathogenesis of psoriasis and the mechanism of action of tazarotene. J Am Acad Dermatol 1998; 39: S129-S133. 4 Weinstein GD, Krueger GG, Lowe NJ et al. Tazarotene gel, a new retinoid, for topical therapy of psoriasis. vehicle-controlled study of safety, efficacy, and duration of therapeutic effect. J Am Acad Dermatol 1997; 37: 85-92. 5 Kligman AM, Willis I. A new formula for depigmenting human skin. Arch Dermatol 1975; 111: 40-48. 6 Kasraee B, Handjani F, Aslani FS. Enhancement of the depigmenting effect of hydroquinone and 4-hydroxyanisole by all-trans-retinoic acid (tretinoin): the impairment of glutathione-dependent cytoprotection? Dermatology 2003; 206: 289-291.