A recent study by Ling et al [16] using a mouse model where mutation in K-Ras G12D was used to induce PDAC showed that this activating K-Ras mutation induced activation of NF-kB, which was required for PDAC development, and expression of IL-1α in the tumor cells and that this create a intrinsic inflammatory response that promote a pro-tumorigenic microenvironment through the expression of inflammatory mediators, e.g. cytokines such as IL-1α [16]. The gene discussed is KRAS; the disease is neoplasm.