It is possible that this microenvironment contributes to the reduction in DROSHA expression in MenSCs, given that alterations in DROSHA are related to inflammatory processes, as previously described, and that the eutopic endometrium of women with endometriosis III and IV presents a sustained stress profile due to the enrichment of TGF signaling pathways, interferon alpha/gamma responses, and the prevalence of natural killer T cells [13]. The gene discussed is DROSHA; the disease is endometriosis.