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. 2017 Jul 17;7:5519. doi: 10.1038/s41598-017-05736-9

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© The Author(s) 2017

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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Schematic of cell survival or cell death defined by the intensity of ROS1 activity. (Left) In the absence of a TKI, mutated CD74-ROS1-expressing cells have the potential for excessive activation of ROS1, so that apoptotic signaling is more intense than survival and growth signaling because of excessive ROS1 signaling, that is, when ROS1 activity is not inhibited. (Middle) Cells survive and grow when the intensity of ROS1 activity is moderately inhibited by low-dose ROS1-TKI. (Right) Cells mainly undergo mitochondria originated initiated apoptosis when ROS1 activity is completely inhibited by high-dose ROS1-TKI treatment.