Meanwhile, suggesting the potential value of anti-TNF-α therapy in CLAD-BOS, it was further reported that classically activated macrophages adjacent to bronchial epithelial cells of lung transplant patients show increased secretion of TNF-α and IL-1β, in parallel with significantly enhanced epithelial-mesenchymal transition (EMT) driven by transforming growth factor beta-1 (TGF-β1) (38). The gene discussed is TNF; the disease is Buschke-Ollendorff syndrome.