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. 2023 Sep 11;13(1):142. doi: 10.1038/s41408-023-00911-w

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© The Author(s) 2023

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. 2 — When treated with a doublet regimen of HMA plus venetoclax (top panel), a population of the FLT3-mutated subclone persists and contributes to relapse. Sequential therapy with gilteritinib is non-curative even in responding patients, and eventually resistance mechanisms contribute to relapse. A triplet regimen of HMA plus venetoclax plus a FLT3 inhibitor (bottom panel) has added synergy that may lead to longer, more durable responses, and possibly cure. The addition of a FLT3 inhibitor not only targets the FLT3-mutated clone, but some FLT3 inhibitors have been shown to increase the sensitivity of leukemia cells to gilteritinib by promoting a more pro-apoptotic phenotype.