Mechanisms of “tumor-promoting inflammation” have been described in PDAC, where activation of oncogenic Kras promotes production of inflammatory cytokines, such as IL-6 and IL-1α, which activate STAT3 and NF-κB, respectively, in an autocrine or paracrine manner to promote tumor cell survival and proliferation, angiogenesis and increased invasive and metastatic behavior of pancreatic cancer cells [6–9]. This evidence concerns the gene STAT3 and neoplasm.