Jak/STAT signaling is normally activated transiently in healthy immune cells however many factors (IL-6, IL-10, TGF-β, VEGF) secreted by pancreatic tumor or stromal cells could lead to constitutive Jak/STAT activation and subsequent differentiation of immunosuppressive populations (Treg, MDSC, Th17) [16–18]. This evidence concerns the gene SOAT1 and pancreatic neoplasm.