ESR1 and breast cancer: These factors not only include synthetic ERα ligand (e.g., fulvestrant and tamoxifen) [6, 7], but also molecules that do not bind to ERα (e.g., emetine, carfilzomib, ouabain, and digoxin) [8, 9, 10, 11] and pathways not directly related to ERα signaling (e.g., endocytic and metabolic pathways) [12, 13, 14, 15, 16, 17], which in turn alter ERα levels and inhibit BC cells proliferation.