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. 2023 Apr 5;37(5):988–1005. doi: 10.1038/s41375-023-01877-1

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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. 6 — All known KMT2A gene rearrangements are subclassified either into reciprocal (balanced) chromosomal translocations (n = 91), spliced fusions (n = 3 + 9), inversion on chromosome 11 (n = 6 + 1), deletions on chromosome 11 (n = 3) and TPG chromatin fragment insertions into the KMT2A gene, or vice versa, KMT2A gene fragment insertions into the TPG’s (n = 12). A few of the possible gene rearrangements are depicted at the bottom where different genetic scenarios are indicated. Since we had analyzed more than 400 complex KMT2A rearrangements, most of these scenarios have been identified, apart from chromotripsis which is a known mechanism to generate a multitude of gene fusions in solid cancer, but not in hemato-malignant tumors.