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. 2021 Feb 24;6:78. doi: 10.1038/s41392-021-00486-7

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© The Author(s) 2021

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. 3 — Roles of alternative splicing in tumorigenesis. The diagram illustrates different hallmarks of cancer along with examples of alternative splicing events that contribute to the transformation of normal cells into tumor cells mainly via proliferation and apoptosis, invasion and metastasis, angiogenesis and metabolism. Arrows up and down indicate the alternative isoforms contributing the most and the least to each process. ITGA6 integrin subunit α6, PKM pyruvate kinase, Bcl B-cell lymphoma, VEGF vascular endothelial growth factor, TAK1 TGF-β-activated kinase 1, CD44 cluster of differentiation 44