One proposed aetiology of acquired endocrine resistance is the gradual expansion of cancer cell populations that are insensitive to ER antagonists.33,34 To test the contribution of PR phosphorylation to acquired tamoxifen resistance, we used naturally occurring PR-null/low variants of ER+ T-47D and PR knock-out MCF-7 breast cancer cells and stably reintroduced either unmodified PR-B or transcriptionally hyperactive (deSUMOylated; K388R) PR-B. This evidence concerns the gene PGR and breast carcinoma.