In agreement with all these findings, we hypothesized that these three major death ligands TNF-α, TRAIL and CD95L might play a key crosstalk role in the inflammation-associated progression of PDAC, all being connected to a prototypic pro-inflammatory transcription factor, such as NFκB, which acts as a potential molecular bridge between tumor cells and inflammatory cells [31,32]. The gene discussed is NFKB1; the disease is neoplasm.