We have recently shown that Fra-1-deficient (Fra-1∆/∆) mice are more susceptible than wild-type (Fra-1+/+) mice to bleomycin-induced fibrosis[12], suggesting that this transcription factor is involved in the regulation of complex genetic networks to maintain cellular homeostasis during bleomycin-induced lung inflammation, injury, and repair processes. This evidence concerns the gene FOSL1 and fibrosis.