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Despite the long\u2010term disease control achieved with immunotherapies in some patients, treatment resistance remains a major cause of disease relapse. Accumulating evidence highlights the tumor immune microenvironment, especially macrophages, as a key contributor to immunotherapy failure in MM. Herein, we identified a subset of MM\u2010associated macrophages with high expression of fibroblast activation protein alpha (FAP\u03b1), defined as FAP\u03b1\n                    <jats:sup>+<\/jats:sup>\n                    macrophages. Clinical data showed that FAP\u03b1\n                    <jats:sup>+<\/jats:sup>\n                    macrophages were enriched in the bone marrow versus peripheral blood of MM patients, and their abundance positively correlated with tumor burden. In MM mouse models, depletion of FAP\u03b1\n                    <jats:sup>+<\/jats:sup>\n                    macrophages significantly boosted the efficacy of anti\u2010PD\u20101\/PD\u2010L1 antibody therapy but not anti\u2010CTLA\u20104 therapy; this combinatorial strategy also exerted enhanced anti\u2010tumor effects in EL4 lymphoma and CT26 colorectal carcinoma models. Mechanistically, FAP\u03b1 stabilized PD\u2010L1 expression by maintaining its N\u2010glycosylation and inhibiting proteasomal degradation, and induced PD\u2010L1 synthesis via promoting vimentin (VIM) phosphorylation at the S72 residue. Additionally, FAP\u03b1\n                    <jats:sup>+<\/jats:sup>\n                    macrophages accelerated T cell senescence by secreting soluble FAP\u03b1. Collectively, our findings demonstrate that FAP\u03b1\n                    <jats:sup>+<\/jats:sup>\n                    macrophages mediate MM immune evasion via dual mechanisms, positioning them as promising therapeutic targets to potentiate anti\u2010tumor immunotherapies.\n                  <\/jats:p>","DOI":"10.1002\/advs.202506239","type":"journal-article","created":{"date-parts":[[2026,1,30]],"date-time":"2026-01-30T12:26:59Z","timestamp":1769776019000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["FAP\u03b1\n                    <sup>+<\/sup>\n                    Macrophages Orchestrate Immune Evasion in Multiple Myeloma by Dual Regulation of PD\u2010L1 and T Cell Senescence"],"prefix":"10.1002","volume":"13","author":[{"given":"Huiyao","family":"Gu","sequence":"first","affiliation":[{"name":"Bone Marrow Transplantation Center the First Affiliated Hospital Zhejiang University School of Medicine Hangzhou 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