Whilst the above study focused on the importance for tumour survival of maintaining intracellular cysteine levels to combat ROS-stimulated death, work with the murine MMTV-PyMT spontaneous mammary cancer model, crossed onto a Gclm−/− background, along with use of the GCL inhibitor buthionine sulfoximine and the TXNRD inhibitor auranofin, indicated that the GSH antioxidant system supports early tumourigenesis and that the TXN system can compensate for depletion of GSH by increasing cystine import via Slc7a11, inferring a level of redundancy [200]. This evidence concerns the gene GCLC and neoplasm.