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Genetic variants that impact the carboxyl-terminal domain of FTL and modify its iron-binding capacity have been linked to the disease hereditary neuroferritinopathy, it is characterized by progressive neurologic symptoms and iron accumulation, particularly in the basal ganglia

This cell cycle arrest is accompanied by profound transcriptional and metabolic rewiring, favoring stress tolerance over proliferation

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These reactions are distinct from the "feeling sick" associated with digestion and require medical attention