Since G9a-mediated repression of E-cadherin in human breast cancer is mediated via interaction with Snail (which controls epithelial-mesenchymal transition during embryogenesis and tumor progression) [27], it is possible that G9a stabilizes the Sox2 protein through coordinated interaction with unidentified co-factors that are exclusively expressed by ER(+) breast cancer cells. The gene discussed is SOX2; the disease is neoplasm.