Similarly, although estrogen activity drives proliferation of ER+ breast cancer cells, a major mechanism underlying the efficacy of anti-estrogen therapies, estrogen activity at cancer cell targets can also promote differentiation and inhibit the epithelial mesenchymal transition, increase intercellular adhesion and thereby reduce invasion, and may reduce cancer stem cell activity [25,26,27], all consistent with anti-tumor activity. The gene discussed is ESR1; the disease is neoplasm.