In view of the present findings of the beneficial effects of pharmacological inhibition, downstream of NRF2 signaling, in thyroid SCC tumor cells in a PDX model, and accumulating evidence of NRF2 as a central player and mediator of chemoresistance [86, 87, 88], we suggest that glutaminase inhibitor, or other drugs being developed to interfere with the KEAP1/NRF2 pathway, should be considered in clinical trials to improve the treatment of patients with advanced thyroid cancer that have an otherwise poor prognosis. The gene discussed is KEAP1; the disease is neoplasm.