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Therefore, the clinical application of cuproptosis strategies needs to be carried out on the premise of establishing a therapeutic window, that is, the Cu ion concentration at the tumor site is below the upper limit of FDX1 reduction capacity, while the circulating Cu level is controlled within the compensatory capacity of ATP7B/ATOX1, to ensure the sufficient aggregation of lipoylated proteins and reduce the toxic accumulation in non-target tissues

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