Non-canonical (i.e., non-SMAD) pathways include signaling through mitogen-activated protein kinases (MAPKs), Src kinases, and JAK2 (Janus kinase-2); these pathways can also be activated by risk factors for pulmonary fibrosis (e.g., cigarette smoke) [54] and converge on the signal transducer and activator of transcription 3 (STAT3), a transcription factor involved in the wound healing response [55]. This evidence concerns the gene STAT3 and pulmonary fibrosis.