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. 2024 Dec 2;9:338. doi: 10.1038/s41392-024-02033-6

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© The Author(s) 2024

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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 8 — Graphic summary. (Top Panel: Normal Erythroid Differentiation) SCF and EPO activate the RAS/ERK/MAPK pathway, supporting and balanced erythroid progenitor proliferation, differentiation, and normal RBC production. (Middle Panel: BRAFi-Enhanced Erythroid Differentiation) BRAF inhibitors (BRAFi) paradoxically amplify RAS/ERK/MAPK signaling, promoting erythroid progenitor proliferation and temporarily delaying differentiation, leading to increased RBC production. (Bottom Panel: BRAF^V600E-Mediated Erythroid Disruption) The constitutive activation of BRAF (BRAF^V600E mutation) disrupts erythroid differentiation, leading to abnormal cell fate decisions and impaired erythropoiesis due to excessive MAPK signaling and hyperactivation of AP-1. Graphic summary was generated with BioRender (https://app.biorender.com/)