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. 2023 Apr 17;11(4):e006070. doi: 10.1136/jitc-2022-006070

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© Author(s) (or their employer(s)) 2023. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.

This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See http://creativecommons.org/licenses/by-nc/4.0/.

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Graphical abstract. pMMR tumors with adequate mismatch repair proteins (MLH1, PMS2, MSH2, MSH6, etc.) are resistant to ICBs. BRD4 inhibition transcriptionally decreases the expression of MMR genes in cancer cells, thus promotes cancers acquiring a mutational profile that could sensitize patients to ICBs. MMR, mismatch repair; pMMR, proficient MMR; dMMR, deficient MMR; BRD4, bromodomain containing 4; ICB, immune checkpoint blockade.