IGF system crosstalk with steroid hormone receptors including ER and PR is extensive; IGF1Rβ enhances ER transcriptional activity24 and IRS-1 is a known ligand-independent (LI) PR-B target gene.19,25 We previously demonstrated ER, PR-B, and IGF1Rβ cooperation within transcriptional complexes at a subset of E2-regulated target genes.26 These data provide a strong rationale for further study of phospho-PR interaction with the IGF pathway in ER+ breast cancer models. The gene discussed is PGR; the disease is breast carcinoma.