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. 2024 Oct 8;32(1):132–143. doi: 10.1007/s12282-024-01640-z

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© The Author(s) 2024

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 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. 2 — Investigator-assessed PFS in patients with PIK3CA/AKT1/PTEN-altered tumors in a the Japan subgroup, and b the global CAPItello-291 population. The hazard ratio was estimated in the Japan subgroup using an unstratified Cox proportional hazards model, and in the global CAPItello-291 population using the Cox proportional hazards model stratified according to the presence or absence of liver metastases and previous CDK4/6 inhibitor use. Tick marks indicate censored data. b New England Journal of Medicine. Turner et al. [16]. Copyright © (2023) Massachusetts Medical Society. Reprinted with permission. AKT1 Akt serine/threonine kinase 1, CI confidence interval, NC not calculable, PFS progression-free survival, PIK3CA catalytic subunit of phosphatidylinositol-3-kinase, PTEN phosphatase and tensin homolog