Because many estrogen-dependent breast cancer cells express both ER-α and ER-β, one plausible meaning of this observation is that FOXO may interact with ER-α and ER-β simultaneously at different FOXO domains, resulting in inhibition of both ER-α and ER-β function in breast cancer cells and suppression of ER-mediated tumor growth and development. This evidence concerns the gene ESR2 and neoplasm.