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. 2020 Oct 28;11:5439. doi: 10.1038/s41467-020-19288-6

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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. 1 — Pro-inflammatory effects mediated by the activation of transcription factors (STAT3), the production of cytokines (e.g., IL-6), the activation of NLRP3 inflammasome and the release of chemokines caused by oncogenic KRAS activation are listed. Representative immune cells in the tumour microenvironment (TME) affected by some of these signals are shown. The dotted line indicates co-occurring mutations.