These investigations suggest that some interleukins (interleukin (IL)1, IL2, IL6, IL8, IL10) and other inflammatory mediators (tumor necrosis factor alfa, interferon gamma, monocyte chemotactic protein-1) could play a main role in the endometriosis pathophysiology, allowing ectopic endometrial cells to implant and grow or triggering a celomic metaplasia etiopathogenic mechanism. The gene discussed is CCL2; the disease is endometriosis.