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. 2020 Dec 17;40(6):1162–1175. doi: 10.1038/s41388-020-01597-1

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 6 — LKB1 activation due to glycolysis inhibition is essential for the antiproliferative activity of EGFR TKI in EGFR^WT NSCLCs by activating AMPK to suppress mTORC1 function. However, cigarette smoke and its ingredient B[α]P represses LKB1 expression by enhancing its promoter CpG island methylation which renders NSCLC cells resistant to EGFR TKI. The addition of AMPK activator metformin can overcome EGFR TKI resistance in response to cigarette smoke exposure in patients with EGFR^WT NSCLC.