FAS and idiopathic pulmonary fibrosis: In fact, in our hands, inhibition of NFATc1 alone failed to promote caspase-3 cleavage and did not sensitize IPF-derived lung fibroblasts to FAS activation, suggesting that NFATc1’s profibrotic function may be limited to the capacity of this transcription factor to support PIM1-promoted myofibroblast differentiation rather than apoptosis resistance.