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Our study is based on a ‘signal transduction’ hypothesis, which relies on the crosstalk between LKB1/AMPK and PI3K/PTEN/Akt signaling at the level of FoxO3A. In particular, LKB1 activates AMPK, which in turn activates FoxO3A, while PTEN inhibits Akt, which in turn inhibits FoxO3A.
