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. This evidence concerns the gene TGFB1 and idiopathic pulmonary fibrosis.