Growing evidence suggests that estrogen, which can induce the expression of c-Myc and IGF-1 and facilitate the binding of ERα to the AP1 site of the IGF-1 and c-Myc promoters to promote ovarian cancer cell proliferation, is a risk factor for epithelial ovarian cancer, and silencing SRC-1 can block inducible c-Myc expression and cell cycle progression [99]. The gene discussed is MYC; the disease is ovarian carcinoma.