Exogenous introduction of IGF‐1R in MCF‐7 breast cancer cells activated PI3K and MAPK pathways, rendered the cells less dependent on ERα signaling and consequently less responsive to tamoxifen as well as to the full ERα‐antagonist fulvestrant.22 Proliferation of long‐term estrogen‐deprived MCF‐7 cells was reported to rely on increased p‐IGF‐1R expression and subsequent PI3K pathway signaling.23 Furthermore, IGF‐1R phosphorylation, but not increased IGF‐1R protein expression, was found to be associated with tamoxifen resistance in MCF‐7 xenografts.24 This evidence concerns the gene ESR1 and breast cancer.