Janssen-Heininger’s group demonstrated the involvement of JNK1-mediated EMT in lung fibrosis as follows: (1) using mouse tracheal epithelial cells from wild-type (WT), JNK1−/−, or JNK2−/− mice, the finding that JNK1 but not JNK2 is required for TGF-β1-induced EMT was shown [62]; (2) accumulated subepithelial collagen deposition associated with the induction of profibrotic molecules, including TGF-β1, in response to a sensitization/challenge with OVA was less in JNK1−/− mice than in WT mice. Here, MAPK9 is linked to pulmonary fibrosis.