C/EBPβ also plays an important role in experimental lung fibrosis, as demonstrated by C/EBPβ null mice that developed less lung fibrosis after bleomycin injury due to the reduced production of lung pro-inflammatory cytokines TGFβ1, TNF-α, and IL-1β, and myofibroblast differentiation [39]. The gene discussed is TNF; the disease is pulmonary fibrosis.