However, the results that estrogen treatment increased both size and number of tumorspheres formed by ER-positive breast cancer cells and CK18 positive cells still underwent estrogen-stimulated cell proliferation suggested that ER-α36-mediated estrogen signaling may stimulate proliferation of breast cancer stem, progenitor and intermediate cells, and also suggested that ER-α36 overexpression might be involved in symmetric stem cell division. This evidence concerns the gene KRT18 and breast carcinoma.