Greater than 50% of ER+PR+ tumors contain ER-PR-K5+ subpopulations  and K5+ cells are increased in ER+ breast tumors following treatment with neoadjuvant endocrine therapy . ER-PR-K5+ luminal breast cancer cell populations, termed ‘luminobasal’ cells exhibiting enhanced progenitor properties can be induced by progestins, glucocorticoids, as well as mineralocorticoids [26, 56–58] and blocked by anti-progestins and prolactin . Interestingly, these K5+ breast cancer cells were found to be less sensitive to 5-fluorouracil and docetaxel in in vitro culture and exhibited reduced apoptosis . A recent study investigated metastasis formation in ovariectomized mice injected with luminal breast cancer cell lines and assessed the metastatic process following treatment with estradiol or estradiol + progestin . The untreated ovariectomized mice were metastasis-free until they were supplemented with estradiol or estradiol + progestin. Unlike the parental cells that were predominately ER+PR+K5- the metastases formed following estradiol or estradiol + progestin contained significantly increased proportions of ER-PR-K5+ cells (6–30%). This finding may have important implications for women on hormonal contraception or replacement therapy who may harbor dormant K5+ micrometastases. It has also been suggested that basal-like breast cancers in BRCA1 deficient women may potentially arise from K5+ luminal progenitors . Compounds that can effectively target these K5+ cells have the potential to improve the outcome of luminal breast cancers and basal-like breast cancers. Targeting K5+ cells may also be effective in reducing recurrence in patients with serous ovarian carcinoma. Indeed many similarities have been observed between basal-like breast cancers and serous ovarian carcinoma .