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. 2021 Mar 1;16:114. doi: 10.1186/s13023-021-01757-w

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© The Author(s) 2021

Open AccessThis 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/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 2 — MicroRNA pathways involved in fetal haemoglobin induction effect of hydroxyurea. Human β-globin cluster consists of a locus control region (LCR) and four function genes (ε,γ,δ and β). γ-Globin is active during fetal life and is suppressed in adults by the action of several transcription factors that include Specificity protein 1 (SP1), Krüppel-like factor 3 (KLF3), Myeloblastosis oncogene (MYB) and B-cell lymphoma/leukaemia 11A (BCL11A). Hydroxyurea alters the expression of several microRNAs (miR) which act on these molecular targets to induce fetal haemoglobin. miR-26b and miR-151–3 stimulate γ-globin at the maximum tolerated dose (MTD) of hydroxyurea