Autocrine signaling is a type of cell regulation in which cells secrete and respond to their particular growth factors. According to fibroblast autoregulated gene expression under SCF gene knockdown and c-kit expression on fibroblasts, the fibroblasts regulated SCF produced in an autocrine manner. Addition of recombinant SCF resulted in a decreased expression level, showing a natural feedback in that the fibroblast cells stopped producing as much SCF . Similarly, adding masitinib inhibited the binding between SCF and c-kit, and so the expression level was increased. The fact that adding both masitinib and SCF produces similar expression levels as the control indicated the automatic balancing of the inner SCF levels, which is the role of an autocrine signaling system. A similar SCF autocrine effect was demonstrated in several tumors . These results further showed the existence of an autocrine system with co-expression of SCF and c-kit in fibroblasts. The present study revealed that although SCF is involved in several processes such as cellular differentiation, proliferation, and survival, it does not influence fibroblast proliferation. Once SCF is silenced in fibroblasts, the autoregulation in gene networks balances the SCF defects in an autocrine regulatory manner. Investigation of the paracrine factors HGF, DKK-1, NRG, CRH, and ET-1 showed HGF exhibited an especially high correlation with SCF. Fibroblasts with SCF dysfunction influenced their own paracrine systems and further affected melanocytes to alter melanin production, particularly under UVB stimulation (Figure 6). Altogether, SCF plays an essential role in fibroblast paracrine factors and in the melanocyte cellular melanogenesis effect.