To address the existence of a potential crosstalk between PR and GR, we used PR+/GR+ breast cancer cell lines (107, 108) where we found that GC-free or DEX-activated GR inhibits PR-dependent cell proliferation and dedifferentiation through the modulation of certain PR-target genes, i.e. GREB1, STAT5A, ELF5 and SNAI1 (8). The gene discussed is NR3C1; the disease is breast carcinoma.