In recent years, it has been suggested that EMs is a systemic auto-inflammatory immune disease and that some immune cells such as macrophages and lymphocytes secrete inflammatory mediators such as IL-8, tumor necrosis factor α (TNF-α), and VEGF that are involved in the pathogenesis of EMs [13]. This evidence concerns the gene CXCL8 and eosinophilia-myalgia syndrome.