The goals were as follows: determine the mechanisms by which the inflammatory environment driven by IL-6 in endometriosis can upregulate miR-21; determine how miR-21 can modulate the TGF-β pathway by the inhibition of Smad7 to enhance fibrosis; and lastly, understand the interplay between the TGF-β pathway/miR21 and CTGF and how they contribute towards endometriosis-associated fibrosis. This evidence concerns the gene IL6 and endometriosis.