Since the development of fibrotic lung lesions is central in the pathogenesis of both CLAD and pulmonary GVHD, and given the afore mentioned advancements in CTGF as a promising therapeutic target in IPF, we tested the hypothesis that CTGF may play a role in CLAD and pulmonary GVHD. This evidence concerns the gene CCN2 and idiopathic pulmonary fibrosis.