Notably, oestrogen-related receptor alpha dependent lactate oxidation renders breast cancer cells resistant to phosphatidylinositol-3-kinase (PI3K) and mammalian target of rapamycin (mTOR) inhibitors cultured in the absence of glucose.39 Additionally, enhanced mitochondrial OXPHOS coupled with suppressed glycolysis is associated with therapeutic resistance to several other targeted therapies in cancer cells.40–42 Overall, these data combined with findings from the present report highlight the importance of metabolic flexibility in cancer cells in response to targeted therapies. Here, MTOR is linked to cancer.