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While tumor\u2010intrinsic mechanisms of endocrine resistance are well established, growing evidence highlights the contributions of innate immune cells and the tumor microenvironment (TME) in shaping therapeutic outcomes. This review synthesizes recent advances into how tumor\u2010associated macrophages (TAMs), natural killer (NK) cells, myeloid\u2010derived suppressor cells (MDSCs), and tumor\u2010associated neutrophils (TANs) collectively foster an immunosuppressive TME that undermines endocrine responsiveness. Central to this crosstalk is the STAT3 signaling pathway, which integrates inflammatory and metabolic stress signals to drive immune reprogramming, promotes tumor progression, and facilitates therapy resistance. By activating tolerogenic pathways and inhibiting anti\u2010tumor immunity, STAT3 provides a mechanistic link between innate immune dysregulation and endocrine resistance. Preclinical studies demonstrate that STAT3 inhibition can restore tamoxifen sensitivity in resistant ER\n                    <jats:sup>+<\/jats:sup>\n                    breast cancer models, highlighting its therapeutic potential. These insights reveal the immunological complexity of endocrine resistance and provide rationale for combinatorial strategies integrating endocrine therapy with immunomodulation. Future approaches that incorporate STAT3 inhibitor, immune checkpoint blockade, and biomarker\u2010guided patient selection may transform the management of ER+ breast cancer, offering more durable and clinically meaningful outcomes by acknowledging the emerging interactions between immune dysregulation and metabolic stress in resistant ER+ breast cancer.\n                  <\/jats:p>","DOI":"10.1002\/ijc.70421","type":"journal-article","created":{"date-parts":[[2026,3,8]],"date-time":"2026-03-08T11:50:48Z","timestamp":1772970648000},"page":"54-66","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Reprogramming innate immunity to overcome endocrine resistance in estrogen receptor\u2010positive breast cancer"],"prefix":"10.1002","volume":"159","author":[{"given":"Siti Nur Hasyila","family":"Muhammad","sequence":"first","affiliation":[{"name":"Department of Chemical Pathology, School of Medical Sciences Universiti Sains 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