Several studies have shown that endocrine therapy resistance in breast cancer cells is modulated by metabolic rewiring and tamoxifen-resistant cells are characterized by HIF-1α hyperactivation via modulation of Akt/mammalian target of rapamycin (mTOR), thus resulting in enhanced aerobic glycolysis and mitochondrial metabolism (15, 16). The gene discussed is MTOR; the disease is breast carcinoma.