Previous studies have detected JAK2/p-JAK2 and STAT3/pSTAT3 levels using quantitative real time-PCR, western blotting, and immunohistochemistry, and the levels of these proteins were observed to be upregulated in the lung tissues of patients with IPF, which demonstrated that phosphorylated STAT3 participates in both lung epithelial cell damage and the fibroblast to myofibroblast transition, making STAT3 an attractive therapeutic target in PF [12, 26]. Here, JAK2 is linked to idiopathic pulmonary fibrosis.