Group I consisted in proteins significantly increased in PLCH compared to SR-ILD or IPF, including well-described mediators of inflammatory chemotaxis as growth-regulated oncogene (GRO)/CXCL1, thymus-and activation-regulated chemokine (TARC)/CCL17 or leptin; and metalloproteinases regulators as tissue inhibitor of metalloproteinases 2 (TIMP-2) (see Additional File 1: Fig. S3). This evidence concerns the gene LEP and idiopathic pulmonary fibrosis.