It has been reported that AKR1B1 could provide tumorigenic and metastatic advantage in basal-like breast cancer through activating the epithelia-mesenchymal transition and enhancing stem cell-like properties (25), and targeting AKR1B1 could depress glutathione de novo synthesis to overcome acquired resistance to EGFR-targeted therapy in lung cancer (26). The gene discussed is EGFR; the disease is breast carcinoma.