SLC7A11 and cancer: In contrast, it was demonstrated that p53 mutants somehow gain additional functional capabilities to inhibit NRF2-mediated transcriptional activation of SLC7A11, resulting in decreased levels of SLC7A11 and GSH and increased ROS and lipid peroxidation in p53 mutant cancer cells, and rendering such tumors more sensitive to SLC7A11 inhibitors such as sulfasalazine (Liu et al., 2017).