In contrast to the acute silencing of PA200 in primary human fibroblasts, we neither observed increased myofibroblast differentiation in chronically PA200-depleted or acutely PA200-silenced primary mouse lung fibroblasts nor any effect on bleomycin-induced lung fibrosis in PA200−/− mice suggesting that PA200 function is possibly species-specific or somehow compensated in these knockout mice as observed in several other knockout strains28. This evidence concerns the gene PSME4 and pulmonary fibrosis.