The higher level of solar elastosis in melasma skin implies that chronic sun exposure is a prerequisite for the development of melasma. After ultraviolet B (UVB) irradiation, keratinocytes induce melanocyte proliferation and melanogenesis by secreting stem cell factor (SCF), basic fibroblast growth factor (bFGF), interleukin- 1, endothelin-1, inducible nitric oxide synthase, a-melanocyte-stimulating hormone, and adrenocorticotropic hormone [19-22]. The secretion of prostaglandin E2 after UVB exposure results in larger and more dendritic melanocytes . Furthermore, the solar damage of the dermis could induce the secretion of melano- genic cytokines, including SCF and hepatocyte growth factor, from the dermal fibroblasts, thereby influencing the development of hyperpigmentation in the overlying epidermis [24, 25]. The dermal fibroblasts secrete a soluble form of SCF during rapid growth or inflammation. Thus, it is possible that the inflammation in the dermis from the accumulated UV irradiation may be associated with the activation of fibroblasts, which can result in the upregulation of SCF in the skin affected with melasma. The SCF mRNA expression is significantly increased in melasma lesions compared with nonlesional skin (0.83 ± 0.5 vs. 0.51 ± 0.4, p < 0.01). RT-PCR of c-kit mRNA also revealed a significant difference in the expression between the lesional and nonlesional skin (0.78 ± 0.7 vs. 0.57 ± 0.6, p < 0.01). Thus, the increased production of soluble SCF in melasma skin is involved via SCF/c-kit-induced signaling in the activation of melanocytes, leading to their increased proliferation and melanogenesis .