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. 2022 Jan 24;13(1):80. doi: 10.1038/s41419-022-04526-0

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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. 8 — Radiotherapy induces cell death in glioblastoma (GBM) and triggers ATP release into the tumor microenvironment (TME). Irradiated GBM cells undergo a P2X7R isoform switch, with overexpression of the truncated P2X7B variant and the downregulation of the full-length P2X7A variant. These radiation-resistant clones are responsible for tumor recurrence.