During the progression of EM, specific anti-inflammatory cytokines (IL-1 beta, IL-5, IL-6, IL-7, IL-12, IL-4, and IL-10) and immune cells (M2 macrophage, neutrophil, M1 macrophage, and activated mast cells) are critical in supporting the persistence, expansion, infiltration, differentiation, angiogenesis, and immune evasion of endometriotic lesions in a multitude of pathogenic ways (34–37). This evidence concerns the gene IL1B and erythema multiforme.