C3a involvement in EM has also been suggested by previous evidence highlighting its correlation with chemokine CCL8 (60), a promotor of the cross-talk between endometrial cells and MCs in the development of EM through the binding to its receptor CCR1, characterized by over-expression in the ectopic endometrium and colocalization with blood vessels in ovarian endometriomas (61). The gene discussed is CCL8; the disease is erythema multiforme.