In this study, we propose that dysregulation of miR-21, driven by the upregulation of IL-6 during the development of endometriosis and consequent activation of STAT3, can modulate TGF-β signaling in endometriotic lesions by amplifying components of TGF-β signaling resulting in the development of fibrosis. Here, TGFB1 is linked to endometriosis.