Recent studies have shown that AMPK activation could suppress tumor cell growth through in-activating mTORC1 [22,42,43], which is mediated through two following ways: by phosphorylation and activation of TSC2 (Tuberous sclerosis protein 2) [44], the mTORC1 negative regulator [44], and by phosphorylation and inactivating of Raptor (regulatory associated protein of mTOR) [45]. The gene discussed is PRKAA1; the disease is neoplasm.