Specifically, when added alone to cultures of primary lung fibroblasts, AXP2258 (which was the most potent MAP3K19 small-molecule inhibitor tested herein) significantly inhibited the proteins levels of both myofibroblast markers in cultures of slow IPF fibroblasts compared with the DMSO control group. This evidence concerns the gene MAP3K19 and idiopathic pulmonary fibrosis.