Under the homeostatic status, some paracrine factors are changed or their expression is induced by cells suffering from different stresses such as UV. SCF plays a potential role in regulating melanogenesis under homeostatic and stimulatory statuses, especially in response to UVB irradiation . It is known that UVB upregulates transcription, increases the expressions of c-kit and SCF, and stimulates melanogenic activity in melanocytes. To understand whether the stimulation with UVB when SCF was silenced would influence the paracrine factors in fibroblasts, an experiment with gene knockdown and then treatment with UVB were performed. The results showed fibroblasts under UVB exposure increase the mRNA expression levels of SCF, HGF, DKK-1, NRG, and CRH related to the melanogenesis gene. Under the same condition, ET-1 was downregulated, as shown in previous studies that reported ET-1 was responsible for a later stage of UVB-induced melanin production. Then, comparison between only UVB-treated and both SCF gene knockdown and UVB-stimulated fibroblasts showed similar results but increasing levels of HGF, NRG, and CRH gene expressions under an SCF-silenced status. Among them, HGF showed more than a 3-fold change compared to only UVB-treated fibroblasts and more than a 20-fold change compared to regular fibroblasts. It was demonstrated SCF was important for UVB-induced paracrine secretion, so HGF needed to strengthen its expression to balance the defect from SCF silencing. In addition, SCF and HGF showed a high correlation in fibroblasts with either UVB stimulation or the homeostatic condition .