Given the effective blocking of molecular pathways leading to lung fibrosis in a Bleomycin model of lung injury and fibrosis by the dominant negative C/EBPβ-Ala217 transgene (Figures 1, 2 and 3) and the anti-fibrogenic effects of a dominant negative C/EBPβ peptide on cultured human lung fibroblasts (Figure 8), we asked whether administration of the peptide could ameliorate the lung injury and fibrosis induced by Bleomycin. The gene discussed is CEBPB; the disease is pulmonary fibrosis.