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An important theoretical concern exists: c-Met is overexpressed in multiple human cancers (gastric, lung, colorectal), and chronic c-Met pathway stimulation could potentially influence cancer riskthough this has not been studied longitudinally even in animals

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A mitochondrial-derived peptide like MOTS-c may be part of that strategy when your symptoms, history, and data point in the same direction, and when it fits alongside the fundamentals that make metabolic change stick