MiR-200 upregulation has been related to the repression of transforming growth factor-beta (TGFb)-induced Epithelial–Mesenchymal Transition (EMT) programs, consistent with non-invasive behavior in ductal in situ carcinomas [44], and with tumor suppressive effects in invasive BC, especially in the setting of TNBC [45,46,47,48]. Here, TGFB1 is linked to ductal breast carcinoma in situ.