However, since uPAR silencing either in melanoma and prostate cancer cells [13] or in ECs and ECFCs is unable to exhaustively inhibit amoeboid movement, we speculate on a possible role of other protease receptors (in particular MMPs receptors), in the light of the recent observation indicating that also MMP9 regulates amoeboid migration of melanoma cells in a catalytic independent manner through regulation of actomyosin contractility via its CD44 receptor [26]. Here, MMP9 is linked to prostate cancer.