CSF1R and Buschke-Ollendorff syndrome: We are particularly intrigued by (a) the potential role of TRM in BOS pathogenesis and rationale for TRM specific therapies; (b) preliminary rationale for CSF1R inhibition in CLAD-BOS; (c) a possible compensatory antifibrotic response in BOS, providing preliminary justification for therapies shifting the balance from a pro- to antifibrotic milieu; and (d) similar transcriptomes in CLAD- and cGVHD-BOS, suggesting a shared pathogenesis and, potentially, common therapeutic targets.