This alteration may be a response to the loss of Dkk-3 in the epithelium, which normally opposes the potential tumorigenic impact of TGF-β by reducing Smad3 phosphorylation in myofibroblasts (Figure 3B); thus, stromal Dkk-3 may contribute to supporting a normal acinar architecture, thereby reducing proliferation and limiting prostate cancer cell invasion [13]. Here, TGFB1 is linked to prostate carcinoma.