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. 2020 Jan 3;11:74. doi: 10.1038/s41467-019-13771-5

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© The Author(s) 2020

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. 8 — a YAP1 was activated when ALK-rearranged cancer cells survived a treatment with ALC. Combinatorial therapy against ALK and YAP1 may achieve complete remission in treatment naïve ALK-rearranged tumors. b A mechanism underlying initial survival against ALC. YAP1 is activated by ALC. Activated YAP1 enters the nucleus and promotes the expression of BCLXL and MCL1. MCL1 and Bcl-xL inhibit apoptosis. Verteporfin inhibits the promoter activity of YAP1, as reported previously.