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If the majority of mutations derive from the mélange of mutagens present in tobacco smoke, the clone of cells that ultimately becomes cancerous would acquire, over its lifetime, an average of one mutation for every 15 cigarettes smoked

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The increased presence of FFAs in the liver activates tumor necrosis factor-α (TNF-α) production in hepatocytes, which in turn inhibits hepatic adiponectin activity and promotes both MASLD and hepatic IR [51]

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