If this results in reduced sensitivity of PDAC-derived cells to TRAIL-induced apoptosis, then the PAR2-TGF-β interaction would be crucially involved in a novel tumor-promoting function of TGF-β—tumor escape from immune surveillance and resistance to TRAIL- or TRAIL-R1-based therapy regimens for treatment of PDAC [33]. Here, TNFSF10 is linked to neoplasm.