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. 2021 Mar 10;6:117. doi: 10.1038/s41392-021-00500-y

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© The Author(s) 2021

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. 4 — Rewired signal pathways by deregulated Myc in cancer and its related components available for synthetic lethality. Input signals, including pro-stability signals from CAMKIIγ or Aurora B kinase, pro-expression signals from IRE1α–XBP1s pathway, and gross genetic changes of Myc, lead to the deregulation of Myc. Multiple pathways, including cell cycle progression, DNA repair, ER stress response, mRNA processing, metabolism, and transcription, were rewired by the output signal from oncogenic Myc to meet its oncogenic needs. Among these Myc-educated signal pathways, some related components indicated here have been verified as synthetic lethal partners of oncogenic Myc