Our results suggested that ZBM improves IPF partly by influencing the trans-differentiation of fibroblasts to myofibroblasts through multiple targets such as EGRF, AKT1, MAPK1, SRC, PIK3CA, MAPK3, and JAK3 and multiple pathways such as the PI3K/AKT, MAPK, and JAK/STAT signaling pathways. The gene discussed is MAPK1; the disease is idiopathic pulmonary fibrosis.