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The body of research on GPX4 is large, and accelerating, as researchers continue to uncover how GPX4 is implicated in human diseases and how inactivation of GPX4 leads to lipid peroxidation-induced ferroptosis

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To assist cancer cells overcome oxidative stress barriers during carcinogenesis, mutations in KEAP1 trigger the nuclear factor erythroid‐related factor 2 (NRF2) antioxidant program and work in tandem with mutant KRAS to drive the development of lung adenocarcinoma (LUAD) [103, 104, 105, 106, 107, 108]