Having discovered that GR inhibited estradiol-activated gene expression and proliferation in wild-type ER+ BC cells, we next examined whether GR similarly inhibited constitutively-active mutant ER activation of CCND1, CDK2, and CDK6. Several labs recently reported that both E2-activated wild-type and non-liganded mutant ER target many of the same enhancer regions [39, 41, 42]. The gene discussed is ESR1; the disease is breast cancer.