MTOR and neoplasm: Tumor glycolysis is enhanced and attenuated by AMP-activated protein kinase (AMPK)-dependent inhibition of mTOR in NSCLC patients who smoke; this in turn inhibits expression of the master kinase of the AMPK subfamily, LKB1, through CpG island methylation, and LKB1 expression was positively correlated with the sensitivity of NSCLC patients to TKIs [41].