These findings raise the possibility that Dkk-3 is a co-factor in the initiation of the angiogenic switch observed in BPH and PCa that is associated with a shift in the ANGPT1/ANGPT2 ratio in favor of ANGPT2. We hypothesize that the loss of the vessel stabilizing factor ANGPT1 (that is highly expressed in the absence of Dkk-3) due to elevated local Dkk-3 levels in endothelial cells and the surrounding stroma, leads to vessel destabilization that favors angiogenic sprouting. This evidence concerns the gene ANGPT1 and benign prostatic hyperplasia.