More importantly, the interactions between prostaglandin E2 (PGE2) and EP2 can produce positive feedback signals to increase TNF-α, IL-6, CXCL1, and COX-2 levels of neutrophils and tumor-associated fibroblasts [87], thereby promoting tumorigenesis by amplifying inflammation and shaping the inflammatory microenvironment [88,89]. The gene discussed is IL6; the disease is neoplasm.