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. 2023 May 15;8:185. doi: 10.1038/s41392-023-01403-w

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© The Author(s) 2023

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 — Proposed working scheme of SYK. a The proposed mechanism by which SYK affects the therapeutic response to c-Metis. SYK regulates the epithelial cell state and is associated with the therapeutic response to c-Metis, while SYK downregulation by TGF-β1 is associated with an enhanced mesenchymal state that confers resistance to c-Metis. b A proposed scheme of SYK stratification to guide clinical decisions related to c-Met-targeted therapy