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This study suggests that, in the context of p53 deficiency, SLC7A11 can promote tumor development through a non-canonical mechanism by directly interacting with ALOX12 and inhibiting ALOX12-mediated ferroptosis, which seems to be independent of its cystine transporting activity (Fig

However, three critical barriers hinder clinical translation: (1) metabolic heterogeneity, where efficacy depends on baseline microbiota (e.g., prebiotics fail in individuals lacking SCFA-producing bacteria)