In this model, the peak5 region is open and enhances sox10 expression in early melanoma precursor lesions and, through a feed-forward mechanism, autoregulates increasing sox10 expression by binding at the dimeric SoxE sites in peak5. An appealing aspect of this type of model is that even stochastic perturbations that increase sox10 binding/activation ability would tend to be reinforced and amplified, potentially “locking in” a sox10 high/pro-NCC program in melanoma. The gene discussed is SOX10; the disease is melanoma.