In mouse models, PDAC is driven by combined oncogenic KRAS mutation and haploinsufficient PTEN deficiency, which together promote marked NF-kB activation, its cytokine network (CCL20, CXCL1, IL-6, and IL-23), stromal activation, and immune cell infiltration; these processes shape the pancreatic cancer tumor microenvironment, stimulate the development of peritumoral stroma, and promote local and metastatic progression (Ying et al., 2011). The gene discussed is KRAS; the disease is pancreatic neoplasm.