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. 2023 Apr 5;72(9):1758–1773. doi: 10.1136/gutjnl-2022-328364

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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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A working model of a tumorous adaptive transcriptional programme to evade immune-checkpoint targeting. During mono-ICB therapy, HCC cells adapt by PPARγ upregulation to orchestrate an MDSC-enriched and T cell-dysfunctional TME via VEGF-A secretion. Selective targeting of PPARγ signalling abrogates the adaptive immune-evasive programme in TME to avert ICB resistance, leading to tumour regression. HCC, hepatocellular carcinoma; ICB, immune-checkpoint blockade; MDSC, myeloid-derived suppressor cell; PPARγ, peroxisome proliferator-activated receptor-gamma; TME, tumour microenvironment; VEGF, vascular endothelial growth factor.