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Finally, the functional redundancy or compensation between iron metabolic regulators in ferroptosis (e.g., whether inhibition of TFR1 can be rescued by enhanced ferritinophagy) has not been rigorously evaluated, which is essential for designing robust therapeutic strategies targeting iron-dependent ferroptosis

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Thus, the ultimate clinical phenotype in a disease where both white matter cytodegeneration and adaptive autoimmune inflammation conspire in the pathogenesis is determined by the vigor of either or both processes, i.e., by a convolution of the two

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