In fact, based on serial immunohistochemistry analyses of ectopic endometrium in a mouse model of adenomyosis, we recently report that activated platelets coincide with TGF-β1 release and the induction of TGF-β/Smad signaling pathway in adenomyosis, as well as evidence of epithelial-mesenchymal transition (EMT) and fibroblast-to-myofibroblast transdifferentiation (FMT), resulting ultimately in fibrosis [10] and also smooth muscle metaplasia (Shen et al., unpublished data). Here, TGFB1 is linked to adenomyosis.