It was shown that AKR1C3 promotes resistance to (1) anthracyclines via carbonyl reductase activity [54,55], (2) paclitaxel in breast cancer via aldehyde metabolism [56], (3) docetaxel in prostate cancer [57], and (4) esophageal adenocarcinoma therapies through ROS/AKT regulation [50]. This evidence concerns the gene AKT1 and esophageal adenocarcinoma.