To further confirm that the estrogen antagonist properties of tamoxifen can be restored to tumor resistance after FASN blockade, we re-examined both the FASN gene regulatory effects of estradiol and/or tamoxifen and the effect of the FASN inhibitor C75 on in vivo tumorigenesis using luminal B-like BT-474 cells, which are ER+, naturally overexpress HER2, and are primarily resistant to tamoxifen, and in endocrine-unresponsive, basal-like MDA-MB-231 cells. Here, FASN is linked to neoplasm.