Multiple mechanisms contribute to the growth of endocrine therapy-resistant breast cancers, including activation of PI3K/AKT and ERK/MAPK signaling, and activation of growth factor receptor signaling such as HER2, EGFR, and IGF-1R.1,6,7 In our present study, PTK6 downregulation in tamoxifen-resistant ER+ breast cancer cells does not alter levels of activated PI3K/AKT, ERK or growth factor receptors, including HER2, EGFR, and IGF-1R (data not shown). The gene discussed is ERBB2; the disease is breast cancer.