As mentioned in previous reports, the reduced inhibition of NF-κB activation meant that along with the existing KRAS and STAT3 cytokine networks, a greater sustained activation of NF-κB ensues.51 PP2A repression also increases the activity of kinases including IKK, JNK, PKC, and ERK, all of which have important roles in accelerating pancreatic cancer progression.50,52–54 In accordance with these reports, this study showed that the cell proliferation of PDAC cells increased when treated with LPS and/or ATP (Figures 1, Figures 5, Figures 6, 7). The gene discussed is STAT3; the disease is pancreatic neoplasm.