Vitiligo is an idiopathic depigmentary skin disorder characterized by selective destruction of melanocytes. Recent observations support the role of altered cellular immunity, autoimmunity, and a role for cytokines in the pathogenesis of vitiligo. The characteristic lesion in vitiligo is a sharply demarcated milky white macule or patch which is surrounded by normal skin. Vitiligo may be divided into localized, generalized and universal. Transforming growth factor beta-1 (TGF-β1) is produced by many cell types including epidermal keratinocytes, TGF-β1 is the main product of regulatory T cells (Tregs). TGF-β1 has an inhibitory effect on keratinocytes, and acts on melanocytes via specific receptors producing paracrine inhibition of human melanocyte proliferation and melanogenesis. vitiligo is an autoimmune disease affecting melanocytes, with a role for Tregs in its pathogenesis, and since TGF-β1 inhibits melanocytes and regulates Tregs, it is expected to have a role in the pathogenesis of vitiligo. In the present study, we examined the degree of expression of TGF-β1 in serum of 24 vitiligo patients and compared this degree of expression with that of 23 normal healthy controls’ serum, using ELISA kit, Serum TGF-β1 was significantly higher in patient with active disease than with inactive disease, so further studies are needed to evaluate the level of TGF- β1 both locally and in serum. And to estimate TGF-β1 level in a larger number of patients to detect if it could be considered a possible marker of disease activity.