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The initiation of breast cancer is associated with increased expression of tumor-promoting estrogen receptor α (ERα) protein and decreased expression of tumor-suppressive ERβ protein.However, the mechanism underlying this process is unknown.Here we show that PERK, an estrogen-inducible protein, can regulate the balance between ERα and ERβ.PERK enhances transcriptional activity of ERα and reduces that of ERβ, and modulates many es-trogen-responsive genes which function in DNA replication and cell cycle regulation.Over-expression of PERK increased ERα homodimerization, and decreased ERβ homodimeriza-tion and ERα-ERβ heterodimerization.