To investigate the individual contribution of NFATc1 and PIM1 to IPF-derived lung fibroblast activation, we first performed RNAi-mediated knockdown of NFATc1 in primary lung fibroblasts derived from 3 independent IPF patients, followed by treatment with TGF-β to enhance their activation. The gene discussed is NFATC1; the disease is idiopathic pulmonary fibrosis.