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Chronic obstructive pulmonary disease (COPD) is responsible for 3.7 million deaths annually, with an increasing global prevalence projected to reach 592 million by 2050.1 2 Contemporary understanding recognises COPD as a heterogeneous syndrome requiring multilevel characterisation across phenotypes (emphysema-dominant, asthma-COPD overlap, early disease states such as pre-COPD, frequent exacerbator), molecular endotypes and measurable biomarkers that together identify treatable traits.3 4 The neutrophil-centric (T2-low) endotype, driven by IL-1β/IL-8/IL-17 pathways, represents the majority and is typically corticosteroid-resistant.5 The eosinophil-predominant (T2-high) endotype, present in 20%–40% of patients and mediated by IL-4/IL-5/IL-13, demonstrates responsiveness to corticosteroids and biologics, with blood eosinophil counts guiding therapy as a continuous biomarker.6 7 This framework has been operationalised through the treatable traits approach8 9 and is embraced in the 2025 GOLD guidelines, which formally integrate biologics such as dupilumab and mepolizumab for patients with elevations in peripheral eosinophils uncontrolled on triple therapy.10 Although approaches based on systemic metrics can identify endotype-appropriate therapies, such approaches are not able to map location and extent of treatable pathology within the heterogeneous lung, or whether affected lung regions harbour reversible disease.