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To the Editor: Chronic lung allograft dysfunction (CLAD) remains a leading cause of late morbidity and mortality after lung transplantation (1). Previously, we reported that fibroblast activation protein (FAP) is selectively induced in activated/pathological fibroblast subsets in CLAD and that quantitative FAP immunostaining in transbronchial biopsies can serve as an early tissue biomarker associated with subsequent CLAD development (2).
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