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Resistance arises from interconnected mechanisms: genetic alterations reactivating the MAPK pathway or bypass cascades (e.g., PI3K\/AKT\/RTK), epigenetic modulation, metabolic reprogramming, and the tumor microenvironment (TME) remodeling. Despite extensive research into these mechanisms, a cohesive framework linking each resistance module to targeted therapeutic strategies is lacking. This review systematically categorizes resistance into intrinsic and acquired subtypes: intrinsic resistance is driven by constitutive molecular traits of\n                    <jats:italic>BRAF<\/jats:italic>\n                    mutant melanoma (e.g., persistent MAPK activation, baseline PI3K\/AKT hyperactivity), while acquired resistance emerges via therapeutic pressure-induced genetic mutations, epigenetic shifts, metabolic reprogramming, or TME modifications. For each identified resistance mechanism, we provide a detailed examination of corresponding therapeutic advancements. These encompass the development of next-generation BRAFi, strategically designed combination therapies, epigenetic modulators, immunotherapeutic approaches, and RNA-based therapeutic agents. Furthermore, we underscore the pivotal role of state-of-the-art technologies, such as liquid biopsies, single-cell multi-omics analyses, and artificial intelligence, in facilitating precise resistance monitoring and personalized therapy selection. By integrating these insights, we present a structured, translationally focused framework to guide basic research and clinical decision-making, ultimately advancing precision salvage therapy and trials aimed at preventing or overcoming BRAFi resistance.\n                  <\/jats:p>","DOI":"10.1186\/s43556-026-00425-4","type":"journal-article","created":{"date-parts":[[2026,3,11]],"date-time":"2026-03-11T01:01:57Z","timestamp":1773190917000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":10,"title":["BRAF inhibitor resistance in melanoma: from resistance mechanisms to therapeutic innovations"],"prefix":"10.1186","volume":"7","author":[{"given":"Yan","family":"Shang","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tingping","family":"Cao","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Junyan","family":"Li","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Juan","family":"Li","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lingnan","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qiqi","family":"Ma","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lanyan","family":"Feng","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hailong","family":"Zhao","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,3,11]]},"reference":[{"key":"425_CR1","doi-asserted-by":"publisher","DOI":"10.3390\/ijms26167910","author":"S Darabi","year":"2025","unstructured":"Darabi S, Stafford P, Braxton DR, Zuazo CE, Brodie TJ, Demeure MJ. 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