To determine whether alternation of glucose metabolism plays a role in the development of acquired resistance to EGFR TKIs, we first established erlotinib-resistant (ER) clones from wt EGFR-expressing NSCLC lines NCI-H322 (H322) and NCI-H292 (H292) and from an activating EGFR mutant-expressing HCC827 lung adenocarcinoma cell line by culturing the cells in increasing concentrations of erlotinib (by 2.5 μM every 2–3 weeks, up to a maintenance concentration of 10 μM for 3 months). This evidence concerns the gene EGFR and non-small cell lung carcinoma.