IL1B and endometriosis: A substantial body of evidence suggests that a large number of mediators, including cell adhesion molecules such as intercellular adhesion molecule-1 (ICAM-1, CD54) and vascular cell adhesion molecule-1 (VCAM-1, CD106) [137] as well as proinflammatory cytokines such as TNF-α, IL1, IL6, and IL8, and chemokines such as MCP-1, play key roles in the pathogenesis of endometriosis.