This comes on the one hand from inhibition of PAR2-driven (independent of TGF-β) invasion in response to activation by serine proteinases including kallekrein-related peptidases and blood coagulation enzymes [39] of the tumor microenvironment and on the other hand from disruption of the PAR2-TGF-β crosstalk. This evidence concerns the gene TGFB1 and neoplasm.