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This presumably occurs to facilitate the re-establishment of migrating cells in their secondary niches to promote secondary growth and is enabled by the overexpression of cell cycle related cyclin-dependent kinase inhibitors p16(INK4a), p21(Cip1) or p27(Kip1) [33]

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Cells also harbor multiple parallel, GPX4-independent antiferroptotic pathways, many of which rely on endogenous radical-trapping antioxidants (RTAs) that directly quench lipid radicals (Fig