The deregulation of glutathione metabolism is broadly identifiable in the majority of cancers as the genes involved in GSH turnover or utilization are under the transcriptional control of classical tumorigenic pathways, primarily the nuclear factor erythroid 2-related factor 2 (NRF2) signalling which drives the antioxidant response and control the transcription of GCL. Here, NFE2L2 is linked to cancer.