Further in vitro studies indicated that oncostatin M was mitogenic, inhibited spontaneous fibroblast apoptosis, induced COL expression by human lung fibroblasts and inhibited TGF-β induced αSMA expression by a subset of IPF lung fibroblasts characterized by the presence of constitutively active Signal Transducer and Activator of Transcription 3 (STAT3; Scaffidi et al., 2002; Pechkovsky et al., 2012). The gene discussed is ACTA1; the disease is idiopathic pulmonary fibrosis.