Endometriosis has been reported to be associated with immune dysfunctions, such as the evasion of endometrial tissues from natural killer (NK) cell-mediated clearance, inflammation in the peritoneal microenvironment, and upregulation of interleukin (IL)-6, IL-8, and tumor necrosis factor (TNF)-α, which promote the proliferation of endometrial cells and neovascularization (5–7). Here, IL6 is linked to endometriosis.