According to the latest pancreatic cancer study, the collaboration of Th1 cell-derived IFN-γ with tumor necrosis factor(TNF) triggers a state of enduring growth arrest in the G1/G0 phase, activates p16 the inhibitor of cyclin-dependent kinase 4a(p16INK4a), and instigates downstream hypophosphorylation of the Rb protein at serine residues, thereby effectuating the senescence of β-pancreatic cancer cells (38) (Figure 1). This evidence concerns the gene IFNG and pancreatic neoplasm.