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. 2019 Dec 9;9:18630. doi: 10.1038/s41598-019-54901-9

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© The Author(s) 2019

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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ERK1/2 is activated after continued TKI treatment in FLT3-mutated AML. (a) Venn diagram of enriched substrate motifs at the two points of treatment in patient #1. (b) Western blot of phospho-ERK1/2 levels on different days (D) of treatment in patient #1. (c) Immunohistochemistry analysis of phospho-ERK1/2 levels of patient #2 at diagnosis (above) and relapse after TKI treatment (below). (d) Immunohistochemistry analysis of phospho-ERK1/2 levels in patient #3 at diagnosis (above) and relapse after TKI treatment (below). *P ≤ 0.05. Scale bar: 5 µm.