Further studies are needed to confirm the underlying mechanisms of this association, but it can be hypothesized that pathological remodeling processes, as, for example, TGF-β signaling pathways or circulating fibroblasts, associated with ILD/IPF (34, 35) or COPD (36–39), may persist or be activated in some patients after LT and thus contribute to the higher risk of RAS. Here, TGFB1 is linked to idiopathic pulmonary fibrosis.