However, since NRF2‐mediated antioxidant responses confer a viability advantage to PTC tumor cells [76, 77], it is plausible that abnormal NRF2 activation may be more frequent, and that targeting the KEAP1/NRF2 pathway (e.g. by glutaminase inhibition) may be beneficial to patients with advanced thyroid cancer other than SCC. The gene discussed is KEAP1; the disease is neoplasm.