Through SCF-targeted siRNA inhibition, we demonstrated HGF, NRG, and CRH gene expressions were significantly increased; especially, HGF gene level had the highest change while DKK-1 and ET-1 gene expressions were decreased. The results demonstrated an autoregulation phenomenon between gene networks, inducing a feedback expression when the SCF gene was silenced in fibroblasts. Cellular autoregulation is frequently observed in gene networks through either negative or positive feedback adjustments . Among them, HGF showed 20-fold high expression in fibroblasts after SCF gene silencing compared with regular fibroblasts. Some experiments demonstrated a similar result that SCF expressed in murine stromal cells was activated and induced an increased expression when treated with extra HGF . This demonstration indicated the relationship between HGF and SCF. Hence, in this case, SCF gene knockdown induced transcription of HGF for facilitating the expression of SCF to balance the gene networks. NRG and CRH involved in melanogenesis also increased their gene expressions under the condition of SCF gene knockdown. On the other hand, DKK-1, a Wnt-antagonist, was downregulated after SCF was inhibited. Gherghe et al. indicated Wnt treatment significantly activated HGF expression in human endothelial progenitor cells . In this case, the Wnt-antagonist DKK-1 was downregulated to avoid the Wnt signaling system inhibition, thereby increasing the expression of HGF. The other downregulated gene, ET-1, was indicated for the mechanism of synergistic effect on ET-1 and SCF that led to melanogenesis. Therefore, SCF inhibition influences ET-1 gene expression.