Finally, signaling of ERK, p38, or AKT that were found to be activated in pulmonary fibrosis (47–49), but they were excluded in our experiments may due to various cytokine action mode, so the details of S100A4 receptor and of molecular mechanisms for the connection of S100A4 with the enzymatic conversion of S1P are topic for future studies. Here, S100A4 is linked to pulmonary fibrosis.