By conditional knockout of TGF-β Receptor II (TβRII) and overexpression of a dominant negative Smad3 in prostate stromal cells in LNCaP DRS xenograft model, we have demonstrated that Smad3-mediated TGF-β signaling in prostate stroma promotes prostate tumor growth and angiogenesis [16, 18] and this stromal TGF-β action is partially mediated by Connective Tissue Growth Factor (CTGF) and Fibroblast Growth Factor 2 (FGF-2) signaling [17, 18]. The gene discussed is SMAD3; the disease is prostate neoplasm.