While several studies have shown that activated PR can antagonise ER, emerging evidence suggests an independent role for PR as a context-dependent driver of advanced ER+ breast cancer phenotypes associated with tumour progression in vitro and in vivo.6–8 In ER+ breast cancer cells, reversible posttranslational modifications such as phosphorylation, ubiquitinylation, and SUMOylation create unique PR species. The gene discussed is PGR; the disease is breast carcinoma.