EGFR and neoplasm: The increased metabolism of glutamine in tumor cells leads to the accumulation of corresponding metabolites, and the metabolites can activate the EGFR downstream signals, including mechanistic Target of Rapamycin (mTOR) (Yang et al., 2017), ERK1/2, STAT3, etc. (Villar et al., 2015; Yang et al., 2017; Vanhove et al., 2019), which become an important reason of the decreased NSCLC sensitivity to EGFR-TKIs.