In line with this evidence, treatment of IPF-derived fibroblasts with the PIM1 inhibitor, AZD1208, promoted staurosporine- and FAS-activating antibody–induced caspase-3 cleavage, suggesting that targeting PIM1 in IPF may facilitate myofibroblast clearance. Here, PIM1 is linked to idiopathic pulmonary fibrosis.