Collectively, these findings suggest that ER or estrogen, and to a lesser extent PR, can promote glycolysis in ER+ cells in order to promote tumorigenesis; however, the precise mechanism(s), the role of specific co-factors present in distinct model systems, and the impact of ER/PR-driven glycolysis in ER+ breast cancer tumorigenesis remain unclear. This evidence concerns the gene ESR1 and breast carcinoma.