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. 2021 Mar 29;14:51. doi: 10.1186/s13045-021-01061-x

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© The Author(s) 2021

Open AccessThis 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/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 2 — PARP inhibitors action mechanisms. Catalytic lethality. a PARP is recruited on single-stand breaks (SSB) and PARylates to recruit base-excision repair (BER) agents to repair SSB. b PARPi are competitive inhibitors of PARP and prevent PARylation from occurring. So, BER systems are not recruited and SSB is not repaired, allowing synthetic lethality. Trapping lethality. c Nascent DNA on replication forks is protected from nuclease action by a BRCA1/2 shield. d Inactivated PARP is locked on SSB; thus, the replication fork gets stale. In BRCA1/2 deficient cells, nucleases have the time to degrade nascent DNA, leading to cell death