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Therefore, the cytoplasmic-free zinc concentration has to be tightly regulated [98] and is buffered to a picomolar level [97], being either transported out of the cell and sequestered into vesicles via ZIP and ZnT transporters, or bound to proteins such as metallothioneins (MTs) [99] (Figure 2A,B)

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By selectively targeting the GSH synthesis using BSO, we found that suppressing the mitochondrial TXN system by inhibiting PANK or knocking down COASY significantly increased ferroptosis (Figure 3, C and D) and mitochondrial lipid peroxidation (Figure 3, E–G)