In both our AI-resistant ER+ BC cell models, we observed high levels of CDK6, p-CDK2 and/or cyclin E1, which are regulators of G1/S-phase transition of the cell cycle, in the resistant cells, indicating that the role of the G1/S cooperative cascades in AI-resistance mechanisms is independent of the source of estrogen. This evidence concerns the gene CCNE1 and breast cancer.