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These include engineering T cells with enhanced expression of antiapoptotic factors such as Bcl-2 or Bcl-xL to confer resistance to AICD, pharmacological inhibition of ferroptosis using small molecules such as ferrostatin-1 or liproxstatin-1 to preserve T-cell viability under metabolic stress, and combination approaches that simultaneously target cell death pathways and immune checkpoint blockade to prolong T-cell survival and sustain antitumor responses [312]

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This halts the process of lipid peroxidation, preserving the structural integrity of the mitochondria

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