Vitiligo, a cutaneous achromia, is poorly understood and is related to three hypothetical pathogenetic mechanisms: autotoxicity (excessive endogenous production of phenol radicals, derived from dopaquinone oxidation into melanin products),1neurological (damage of end-terminal portions of autonomic nerves)2 and immunological (anti-tyrosinase and TRP-2 autoantibodies, as well as through activation of cellular immunity).3,4. The gene discussed is TYR; the disease is vitiligo.