Our in vitro data show that NFATc1 silencing or inhibition of its nuclear translocation in IPF fibroblasts limited PIM1 profibrotic functions and blocked TGF-β–promoted fibroblast activation, thus establishing a fibrogenic function for NFATc1 besides its involvement in fibroblast proliferation. The gene discussed is PIM1; the disease is idiopathic pulmonary fibrosis.