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. 2020 Dec 28;81(3):317–331. doi: 10.1007/s40265-020-01461-2

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© The Author(s) 2020

Open AccessThis article is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License, which permits any non-commercial 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-nc/4.0/.

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Fig. 1 — Mechanism of action of CDK4/6 inhibitors. The CDK4/6-cyclin D1 complex induces phosphorylation of the retinoblastoma (Rb) tumor-suppressor protein. Free transcription factor E2F stimulates cell transition from the G1 to the S phase and cell division. AKT protein kinase B, CDK4/6 cyclin dependent kinase 4 and 6, ER estrogen receptor, E2F transcription factor family, HER2 human epidermal growth factor receptor-2, PIK3 phosphoinositide 3-kinase, Rb retinoblastoma tumor suppressor protein, mTOR mammalian target of rapamycin