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The authors show that the drastic growth arrest of the sir1 mutant is partially rescued when glutathione deficiency is introduced via the cad2 mutation, which decreases glutathione levels to 30% to 40% of wild-type levels (Cobbett et al., 1998), or pharmacologically through treatment with the GCL inhibitor buthionine sulfoximine

Since one key cannot unlock every lock, it will be important to decipher context-specific regulatory mechanisms that may ultimately facilitate tissue-specific or cell type-specific interventions on the ferroptotic process in multiple distinct diseases