Interestingly, cells depleted of PAR2 protein lost the ability to autoinduce TGF-β1 at both the mRNA and protein level in response to stimulation with exogenous TGF-β, suggesting that inhibiting PAR2 expression or function is a suitable strategy to interfere with a TGF-β autostimulatory loop in the tumor tissue. Here, TGFB1 is linked to neoplasm.