Previously, we observed that C75-induced FASN inhibition works as a potent antagonist of E2- and tamoxifen-dependent ERα-driven transcriptional activation in human endometrial adenocarcinoma cells.72 We now demonstrate that C75-regulated MAPK/ERK signaling activation, PI3K/AKT pathway inhibition, and ERα signaling work together to promote disruption of human breast cancer cell growth and survival. The gene discussed is ESR1; the disease is breast carcinoma.