In conclusion, we have found that Nintedanib target pathways (PDGF-AA, PDGF-BB, FGF-2, VEGF and M-CSF) are augmented in all PF-ILD subsets and importantly their concentrations are similar across PF-ILD subsets suggesting that Nintedanib treatment should have similar efficacy in PF-ILD regardless of aetiology (e.g., IPF, SSc-ILD and other PF-ILD). The gene discussed is CSF1; the disease is idiopathic pulmonary fibrosis.