The DKK1-SE recruits JUND and FOSL2 through AP1 binding motifs on the core component e1 to initiate chromatin remodeling, induce enhancer and DKK1 promoter to form an active transcription complex to enhance the transcription activity of DKK1. Malignant phenotype analysis and xenograft mouse models showed that deletion of DKK1-SE could alleviate the progression of pancreatic tumors, particularly by reducing the induction of vascular endothelial cells, collagen fibers, and myofibroblasts in the tumor microenvironment. The gene discussed is FOSL2; the disease is neoplasm.