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Our prior genome\u2010wide association study (GWAS) identified\n                    <jats:italic>ANKS1B<\/jats:italic>\n                    as a significant shared genetic risk factor for heroin, methamphetamine, and alcohol dependence, suggesting a broad role in addiction vulnerability. However, the specific function of ANKS1B in cocaine addiction and its associated neural mechanisms were unknown. Here, we found that ANKS1B expression level in the Nucleus Accumbens (NAc) was downregulated after extended cocaine use, and manipulating ANKS1B could selectively influence the escalation of cocaine intake and the subsequent cocaine\u2010seeking behavior in the long\u2010access cocaine self\u2010administration rat model. Molecular experiments reveal that ANKS1B interacts with the histone acetyltransferase CBP to control H3K27 acetylation and extended cocaine intake, via epigenetically repressing the transcription factor FoxO3. Overall, these findings suggest that ANKS1B is a crucial factor influencing the escalation of cocaine use. The ANKS1B\u2010CBP\u2010FoxO3 signaling pathway presents a promising target for potential therapeutic interventions for controlling extended cocaine use.\n                  <\/jats:p>","DOI":"10.1002\/advs.202522949","type":"journal-article","created":{"date-parts":[[2026,6,2]],"date-time":"2026-06-02T14:53:09Z","timestamp":1780411989000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["ANKS1B in the Nucleus Accumbens Controls Escalated Cocaine Self\u2010Administration via Regulating CBP\u2010FoxO3 Complex"],"prefix":"10.1002","volume":"13","author":[{"given":"Liping","family":"Yang","sequence":"first","affiliation":[{"name":"Department of Neurobiology School of Basic Medical Sciences National Institute on Drug Dependence Peking University  Beijing China"},{"name":"Beijing Key Laboratory of Drug Dependence Research Peking University  Beijing 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