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After ingestion, AFB1 is oxidized into a reactive electrophile that alkylates DNA, forming bulky lesions such as the genotoxic formamidopyrimidine lesion, AFB1-Fapy dG. This lesion is mainly repaired by nucleotide excision repair (NER) in bacteria; however, in humans the picture is less clear. We report a plasmid-based host cell reactivation assay containing a site-specific AFB1-Fapy dG lesion and present evidence that this lesion is mainly repaired by transcription-coupled NER (TC-NER) in human cells. Using a combination of isogenic knockout cell lines and immortalized fibroblasts from xeroderma pigmentosum and Cockayne syndrome patients, we show that the TC-NER factors CSA, CSB, and UVSSA are required for efficient AFB1-Fapy dG repair, while the global-genome NER protein, XPC, is dispensable. Furthermore, knockout of CSB or UVSSA impairs AFB1-Fapy dG repair to a similar degree as knockout of the core NER nuclease, XPF. Our data indicate that TC-NER is the major repair pathway for AFB1-Fapy dG adducts in human cells.<\/jats:p>","DOI":"10.1093\/narcan\/zcaf030","type":"journal-article","created":{"date-parts":[[2025,8,30]],"date-time":"2025-08-30T11:58:30Z","timestamp":1756555110000},"source":"Crossref","is-referenced-by-count":1,"title":["The\u00a0aflatoxin B1-induced formamidopyrimidine adduct is repaired by transcription-coupled nucleotide excision repair in human cells"],"prefix":"10.1093","volume":"7","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4529-2302","authenticated-orcid":false,"given":"Daniel\u00a0J","family":"Laverty","sequence":"first","affiliation":[{"name":"Harvard T.H. 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