Indeed, we find that IL-17A promotes pulmonary fibrosis through the activation of PIK3CA to interrupt the GSK3B-mediated degradation of BCL2 and suppress autophagy in lung epithelial cells [19], whereas IL-17A induces hepatic fibrosis through activating the STAT3 pathway and interfering with the p62 mediated autophagy flux in fibrotic liver tissue. Here, BCL2 is linked to pulmonary fibrosis.