The present work demonstrates that AKR1B10, AKR1C1, AKR1C2 and AKR1C3 are transcriptional targets strongly indicative of NRF2 status in human tumours, and that NRF2 is the upstream effector of AKR overexpression in cancer, particularly in tumours of squamous origin. This evidence concerns the gene AKR1C3 and neoplasm.