In pancreatic cancer, hypoxia-induced HIF-1α bound to the HRE of chemical chemokine 2 (CCL2) and increased its expression, recruiting macrophages to infiltrate tumor tissues to activate pancreatic stellate cells and confer it fibroblast phenotypes via increasing the expression of α-smooth muscle actin, aggravating the hypoxic microenvironment of pancreatic cancer and accelerating its progression [85]. This evidence concerns the gene HIF1A and pancreatic neoplasm.