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. 2023 Feb 24;23(6):2687–2694. doi: 10.1007/s10238-023-01017-0

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© The Author(s) 2023

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/.

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Fig. 3 — A Multiparametric flow cytometry analysis of bone marrow cells. Automatic population separator (APS) plot provided the best cell cluster separation, to confirm the identity of CD4+ and CD8+ T cells. Grey color: other nucleated populations. B Human Phospho-kinase Array. Levels of phosphorylated proteins were quantified with Kodak Molecular Imaging Software version 2.0.0 (Eastman Kodak Co., Rochester, NY). A and B representative cases of 6 independent experiments from idiopathic aplastic anemia and benign anemia cases. C The finding of the heterozygous variant (p.520T>C, p.Cys174Arg) in the coiled-coil domain of STAT1 gene, showing gain of function (GOF) activity paved the way for idiopathic aplastic anemia cases investigation. A boosted STAT1 pathway activation unleashes a Th1 phenotype differentiation, driving a variable clinical phenotype, including bone marrow failure. Created with BioRender.com, Publication license n. YK250GFR64