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. 2018 Feb 23;3:5. doi: 10.1038/s41392-018-0008-7

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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. 3 — Various strategies to target Myc. Inhibitors of BRD4, CDK7, and CDK9 inhibit MYC expression at the transcriptional level. Inhibition of the PI3K/AKT/mTOR pathway blocks MYC translation, whereas USP7, AURKA, and PLK1 inhibitors destabilize Myc at the posttranslational level. 10058-F4 and Omomyc function to interrupt the Myc–Max dimeric complex. BRD4 bromodomain-containing 4, CDK7 cyclin-dependent kinase 7, CDK9 cyclin-dependent kinase 9, PLK1 polo-like kinases 1, PI3K/AKT/mTOR phosphatidylinositol 3-kinase/AKT/mammalian target of rapamycin