To explore the therapeutic potential of interrupting the PIM1 signaling pathway in a more relevant disease setting, we developed organotypic cultures from human IPF lungs ex vivo and tested the capacity of PIM1 and NFATc1 inhibitors to attenuate profibrotic gene expression in these explants in the presence or absence of TGF-β (Figure 7A). Here, PIM1 is linked to idiopathic pulmonary fibrosis.