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Although limited studies have been conducted on the detailed mechanisms of OS action in endometriosis-associated infertility, it can be generalized that the excess of ROS results in multi-faceted alterations, including the enhanced production of pro-inflammatory molecules such as interleukine-6 (IL-6), tumor necrosis factor-alpha (TNF-α), or IL-1β, as well as immune shifts toward the predominance of the pro-inflammatory state, alterations in vascular endothelial growth factor (VEGF) production, and increased proliferation through mitogen-activated protein kinase (MAPK) pathway stimulation [27,28]