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Owing to hypermethylation of the promoter, RIPK3 is silenced in primary tumours but significantly upregulated in recurrent lesions, with an enhanced dependence on cysteine metabolism, suggesting that targeting RIPK3 may inhibit tumour recurrence [56]
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Recent reviews reaffirm this “double-edged sword” paradigm and highlight context-specific thresholds and localization of ROS as key determinants of outcome [13]
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