The discrepancy observed between Fra-1Δ/Δ mice (which develop more fibrosis) and Fra-1 transgenic mice (which develop more hepatic fibrosis and interstitial lung disease) could be attributed to a different transcriptional response induced by pro-inflammatory and pro-fibrotic agents in the absence, or in the presence (overexpression), of Fra-1. This evidence concerns the gene FOSL1 and fibrosis.