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 Vascular smooth muscle cell (VSMC) diversification drives atherosclerotic coronary artery disease (CAD), but the mechanisms governing these cell state transitions remain unclear. We applied multiomic single-cell profiling, epitope mapping, and spatial transcriptomics across 27 human coronary arteries, identifying fibroblast activation protein (FAP) as a marker of modulated VSMCs. Lineage tracing in mice indicated that FAP\n                    <jats:sup>+<\/jats:sup>\n                    cells originate from\n                    <jats:italic toggle=\"yes\">Myh11<\/jats:italic>\n                    <jats:sup>+<\/jats:sup>\n                    VSMCs, and FAP positron emission tomography imaging in CAD patients showed plaque uptake. FAP\n                    <jats:sup>+<\/jats:sup>\n                    cell states resided in the macrophage-rich neo-intima. Therapeutically, we developed an anti-FAP bispecific T cell engager, which reduced plaque burden and remodeled the stromal\u2013immune microenvironment through T cell clonal expansion. Our study delivers a single-cell and spatial atlas of human CAD, establishes FAP as a marker of modulated VSMCs, and highlights immunotherapy for lipid-independent targets.\n                  <\/jats:p>","DOI":"10.1126\/science.adx1736","type":"journal-article","created":{"date-parts":[[2026,1,29]],"date-time":"2026-01-29T18:59:16Z","timestamp":1769713156000},"update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark","source":"Crossref","is-referenced-by-count":32,"title":["Targeting modulated vascular smooth muscle cells in atherosclerosis via FAP-directed immunotherapy"],"prefix":"10.1126","volume":"392","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6851-0168","authenticated-orcid":true,"given":"Junedh M.","family":"Amrute","sequence":"first","affiliation":[{"name":"Center for Cardiovascular Research, Division of Cardiology, Department of Medicine, Washington University School of Medicine, Saint Louis, MO, USA."},{"name":"Amgen, South San Francisco, CA, 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