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. 2018 Dec 17;16:360. doi: 10.1186/s12967-018-1729-7

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© The Author(s) 2018

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 2 — This schematic demonstrates the potential mechanisms of escape from JAK2 inhibition by ruxolitinib. (1) Ineffective JAK inhibition (2) Acquired tyrosine kinase domain mutation (3) Heterodimerization of JAK2 with JAK1 or TYK2 (4) Alternative signaling cascade activation (5) External cytokine effects (6) Epigentic mechanisms of transcriptional regulation