PR bound to ERα to direct ERα chromatin binding events at cyclin D1/MYC promoters within breast cancer cells, leading to a unique gene expression program, which was associated with good clinical outcome in the presence of the agonist ligands and blockage of ERα with the pure anti-estrogen fulvestrant disrupted the interaction between ERα and PR in vitro and suppressed MPA-dependent tumor growth in vivo [45]. The gene discussed is ESR1; the disease is neoplasm.