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. 2022 Nov 16;54(11):1814–1821. doi: 10.1038/s12276-022-00887-w

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© The Author(s) 2022

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. 1 — PTEN function can be compromised via genetic disruption, which results in a stepwise loss of PTEN (50% or 100%). Posttranslational modifications, including ubiquitination and deubiquitination, of PTEN can fine-tune PTEN functionality via a continuum of tumor suppression. Notably the phenotypes acquired throughout the continuum of functional PTEN loss are differentially manifested depending on tissue type.