In lung cancer, metastasis rates are increased by upregulated metabolic pathways, such as hexokinase 2 (HK2) and glyceraldehyde-3-phosphate dehydrogenase (GAPDH), in a BACH1-dependent manner, which is further stabilized by an antioxidant treatment or activated nuclear factor-erythroid factor 2-related factor (NRF2) (equivalent to the mutation of Kelch-like ECH associated protein 1 (Keap1)) [13,14]. The gene discussed is GAPDH; the disease is lung carcinoma.