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. 2021 May 31;12(6):561. doi: 10.1038/s41419-021-03844-z

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© The Author(s) 2021

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. 7 — When gefitinib resistance occurs, the cancer cells would try to break through the EGFR/STAT3 signaling pathway. Due to the persistent inhibition of EGFR by gefitinib, they had to compensatively activate other signaling pathways which pass through STAT3. Blocking STAT3 activation by LL1 can reactivate the efficacy of gefitinib.