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Redox metabolism abnormalities in autistic children associated with mitochondrial disease

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A prominent example is their inhibition of the PI3K/Akt pathwayGA treatment in lung cancer cells led to downregulation of PI3K/Akt alongside increased p53 levels, which in turn activated downstream executioner caspases and cell cycle inhibitors (p21Cip1/p27Kip1), culminating in apoptosis and growth arrest (151)