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These findings suggest that ferritinophagy-derived iron and TFRC-mediated endolysosomal iron trafficking may converge within lysosomes to create a vulnerable pool of catalytic Fe 2+ able to initiate ferroptotic damage when properly engaged, thereby linking iron storage turnover, stem-like phenotypes, and ferroptosis sensitivity [36]

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During this process, instead of ADH, cytochrome P450 2E1 (CYP2E1) is activated in the liver to break down acetaldehyde [6]

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Conclusion: The primary goal was to improve patients access to rifaximin, which was achieved with 100% success for those requiring a PA or PAP