The release of interleukins and prostaglandins from tumor-associated macrophages (TAMs), which are recruited and generated locally by inflammation in the prostate gland, not only inhibits the antitumor immune response but also promotes tumor vascularization via the secretion of angiogenic factors such as Endothelin-2 and vascular endothelial growth factor (VEGF), thus further driving the progression of PCa [43]. This evidence concerns the gene EDN2 and neoplasm.