Many growth factors and inflammatory cytokines implicated in lung fibrosis, including the TGF-β1, are known regulators of the AP-1 activity both in vitro and in vivo[10], [11]; however, the exact relevance of Jun and Fos family member activation in pro-fibrotic stimuli and their contribution to lung fibrosis are largely undefined. This evidence concerns the gene JUNB and pulmonary fibrosis.