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. 2019 May 24;33(7):1543–1556. doi: 10.1038/s41375-019-0490-0

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© The Author(s) 2019

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 — Autophagy in CML. The interaction of P210^BCRABL1 with PI3K-AKT inhibits autophagy. Contrariwise, TKIs inhibit kinase activity of P210^BCRABL1 enhancing autophagy. These autophagy effects may kill CML progenitor cells but may preserve CML LSCs