The nature of the interaction between Dkk-3 and TGFBI and their potential signaling crosstalk is complex and possibly tissue-specific, with reduced expression of Dkk-3 in prostate cancer leading to increased expression and secretion of TGFBI [13] and the binding of TGFBI inhibiting the effects of Dkk-3 on integrin-dependent adhesion in hepatocellular carcinoma [43]. This evidence concerns the gene TGFBI and prostate carcinoma.