KEAP1 and neoplasm: Since increased NRF2 activity, resulting from NFE2L2 or KEAP1 mutations, sensitizes tumor cells to glutaminase inhibition, which reduces the bioavailability of glutamine otherwise serving as an antioxidant fuel for tumor growth and survival [6, 27, 28, 29, 30], mice bearing P3 xenografts were treated daily with CB‐839, a seective glutaminase inhibitor (GLSi) currently being evaluated in clinical trials with KEAP1/NRF2 mutant nonsmall cell lung cancer patients [31].