When ER+ breast cancer cells were co-cultured with fibroblasts, reactive oxygen species (ROS) produced by tumor cells in response to tamoxifen treatment drove aerobic glycolysis in fibroblasts; the excess of lactate produced by CAFs induced mitochondrial biogenesis in the adjacent tumor cells, forcing them to switch towards an oxidative state; this metabolic state, with glycolytic CAFs fueling the oxidative tumor cells, sustained anabolic growth and tumor survival in the presence of tamoxifen [90]. This evidence concerns the gene ESR1 and breast carcinoma.