Importantly, in addition to NRF2-directed overexpression of antioxidant enzymes, other mechanisms can be utilized to increase GSH during the later stages of cancer development including, for example, increased generation of NADPH via the folate pathway during metastasis [201] and activation of mTOR signalling as well as increased mitochondrial metabolism and glutamine flux stimulated by estrogen-related receptor α (ERRα) in lapatinib-resistant breast cancer cells [202]. The gene discussed is NFE2L2; the disease is breast cancer.