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. 2018 Apr 7;32(8):1818–1822. doi: 10.1038/s41375-018-0032-1

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© The Author(s) 2018

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. 2 — Integration of genomic, phosphoproteomics, and mass cytometry data to rationalize kinase inhibitors sensitivity. a Viability of AML cells within the indicated genotype/phenotype groups after treatment with MEKi. b Sensitivity of NRAS/BRAF/CDs+ positive cells to MEKi as a function of the indicated factors. c FLT3/PKCi sensitivity of AML cells with the indicated phenotype/genotype. Phosphorylations are denoted as (hi) and (lo) based on a greater or lower phosphorylation than the median across all cases. Significance was assessed by Mann–Whitney test